bluuebunny/crossref_metadata_2025 huggingface dataset:
Relation between capillary pressure and vascular tone over the range from maximum dilatation to maximum constriction in cat skeletal muscle
Authors: MASPERS M. , BJÖRNBERG J. , MELLANDER S.
Published: December 2008

An attempt was made to assess, from a large sample (n = 567), the normal level of hydrostatic capillary pressure (P,) in resting skeletal muscle and the extent of P, regulation as effected by strictly graded activation of metabolic and adrenergic control mechanisms over the entire physiological range of vascular tone. With the use of a new whole‐organ technique, P, towards the venous end of the capillary was continuously recorded at constant arterial pressure (100 mmHg) and under simultaneous observations of total regional vascular resistance (RT), precapillary resistance (R,) and post‐capillary resistance (RV). In the control state with a Starling fluid equilibrium, a venous pressure of 7 mmHg and normal vascular tone (R, = 19.1 ±.3 PRU), P, averaged 16.7 ± 0.3 mmHg. Graded metabolic dilatation (muscle exercise), decreasing RT, to a minimum value of 1.7 PRU, caused progressive increase in Pc, up to 32 mmHg and consequent fluid filtration. Conversely, graded adrenergic constriction, increasing R, to a maximum of 100 PRU, caused a progressive decrease in Pc, down to 10 mmHg and consequent fluid absorption. The relation between P, and R, was highly non‐linear, 4, increasing more steeply the more R, approached low values, and was described by the power function: Pc. = 36.43 x RT‐0.27 (r = ‐0.79, P < 0.001). The resistance ratio, Rv/Ra, (the main determinant of Pc,) and vascular tone (RT,) showed a similar non‐linear relation. Regulatory change of Rv/Ra, was mainly accomplished by active change of Ra but a pronounced Rv decrease (venodilatation) occurred in the lowest R, range, exerting a protective function against excessive increase in Pc, and detrimental plasma fluid loss.
Protein secretion in salivary glands of cats in vivo and in vitro in response to vasoactive intestinal peptide
Authors: EKSTRÖM J. , TOBIN G.
Published: December 2008

In anaesthetized cats exogenous vasoactive intestinal peptide failed to elicit any secretion of saliva from the submandibular and parotid glands. However, protein release from both glands occurred in response to VIP in the presence of α‐ and β‐adrenoceptor blocking agents and was dose‐dependent. This response was revealed by means of a subsequent washout flow of saliva evoked by intravenous injections of methacholine or stimulations of the parasympathetic innervation. The submandibular glands responded to vasoactive intestinal peptide at a lower dose than the parotid glands. In the presence of atropine (but in the absence of adrenoceptor blockers), stimulation of the parasympathetic chorda‐ngual nerve, which of itself elicited no secretion of saliva, contributed to the release of protein within the submandibular gland, since the output of protein in response to a subsequent stimulation of the sympathetic innervation was increased. Vasoactive intestinal peptide administered in combination with methacholine or during ongoing parasympathetic nerve‐induced salivary secretion revealed positive interactions, particularly with respect to protein release. In‐vitro protein release in response to vasoactive intestinal peptide was also demonstrated by perifusing small pieces of the two glands in the presence of muscarinic and adrenoceptor blockers. As in vivo, submandibular tissue responded at a lower concentration of vasoactive intestinal peptide than the parotid tissue. One to two weeks after combined parasympathetic and sympathetic denervation of the parotid glands, the glands were sensitized to vasoactive intestinal peptide when tested in vitro. It is concluded that vasoactive intestinal peptide or a structurally related peptide is a potential transmitter in the parasympathetic control of protein secretion in salivary glands of cats.
Loop diuretics reduce lithium reabsorption without affecting bicarbonate and phosphate reabsorption
Authors: STOKKE E. S. , ØSTENSEN J. , HARTMANN A. , KIIL F.
Published: December 2008

The effects of the loop diuretics ethacrynic acid and bumetanide on lithium, bicarbonate and phosphate reabsorption were compared in 16 anaesthetized, normovolaemic dogs. In six dogs, ethacrynic acid (3 mg kg‐1body wt) significantly reduced absolute lithium reabsorption from 29.3 ± 4.1 to 19.0 ± 3.4μmol min‐1, fractional lithium reabsorption from 0.65 ± 0.04 to 0.37 ± 0.04 and fractional chloride reabsorption from 1.00 ± 0.00 to 0.65 ± 0.02. Bicarbonate and phosphate reabsorption did not decrease significantly. In six other dogs, bumetanide (30 μg kg‐1body wt) gave similar results. Absolute lithium reabsorption significantly decreased from 34.0 ± 2.2 to 18.1 ± 2.6 μmol min‐1and fractional lithium reabsorption decreased from 0.50 ± 0.03 to 0.25 ± 0.03. Fractional chloride reabsorption decreased from 0.98 ± 0.00 to 0.61 ± 0.05, whereas bicarbonate and phosphate reabsorption were not significantly altered. Thus, both loop diuretics greatly reduced lithium reabsorption. We propose that loop diuretics inhibit passive lithium reabsorption in the thick ascending limb of Henle's loop by reducing the lumen‐positive electrical potential that drives passive cation transport.
Atrial natriuretic peptide during head‐up tilt induced hypovolaemic shock in man
Authors: MATZEN S. , KNIGGE U. , SCHÜTTEN H. J. , WARBERG J. , SECHER N. H.
Published: December 2008

To evaluate the importance of right atrial filling pressure versus central blood volume for the plasma concentration of atrial natriuretic peptide in man, head‐up tilt to 50± maintained until the appearance of presyncopal symptoms was carried out in six healthy males. Head‐up tilt increased thoracic electrical impedance from 35± 0.9 (mean and SE) to 39.2 ± 0.9 ohm, mean arterial pressure from 64.5 ± 3.6 to 76.6 ± 3.0 mmHg and heart rate from 51± 3 to 85 ± 4 beats min‐l (P < 0.01). After 35 ± 7 min presyncopal symptoms appeared, together with a decrease in mean arterial pressure to 51 ± 4 mmHg and in heart rate to 59 ± 7 beats min‐1 (P < 0.01). Central venous pressure (2.1 ±1.0 mmHg) did not change significantly, but atrial natriuretic peptide decreased from 9.4 ± 1.6 to 4.2 ± 1.3pmol l‐1 (P < 0.01) and was inversely related to thoracic impedance (r= ‐0.65, n= 44, P < 0.001). The results indicate that changes in the central blood volume rather than in central venous pressure determine the secretion of atrial natriuretic peptide in man.
Haemodynamic information encoded in the aortic baroreceptor discharge during haemorrhage
Authors: HARTIKAINEN J. , AHONEN E. , NEVALAINEN T. , SIKANEN A. , HAKUMÄKI M.
Published: December 2008

This study concerns the function of aortic baroreceptors during slow haemorrhage, in particular the mechanisms by which baroreceptors respond to hypovolaemia in the absence of hypotension and the manner in which haemodynamic information is encoded in the aortic nerve discharge. Beagle dogs, anaesthetized with morphine and chloralose, were instrumented for the recording of aortic pressure, aortic diameter, aortic flow and aortic nerve activity. The animals were subjected to slow haemorrhage (0.4 ml kg‐1 min‐1) of 20% of the estimated blood volume. Mean aortic pressure remained unchanged, whereas mean aortic diameter, mean aortic tension and aortic baroreceptor activity decreased during the haemorrhage. Baroreceptor sensitivity to mean aortic pressure, mean aortic diameter and mean aortic tension decreased as the haemorrhage proceeded. Also, the sensitivity of baroreceptors to mean aortic pressure and mean aortic diameter during acute pressure stimulation was attenuated. The results indicate that during non‐hypotensive haemorrhage aortic baroreceptor discharge is reduced by two mechanisms: firstly, via constriction and stiffening of aortic smooth muscle and, secondly, via direct effects of the compensatory mechanisms on the baroreceptors. The reduced sensitivity renders the baroreceptors capable of responding to hypovolaemia prior to the onset of hypotension. In the regression analysis, systolic aortic diameter proved to be the best determinant of baroreceptor activity (r = 0.877). Of the neural variables, impulses per cardiac cycle and average discharge rate were the most reliable, but no difference in the relative importance of these two parameters could be observed.
Simultaneous recordings of cytosolic Ca2+ level and membrane potential and current during the response to thyroliberin in clonal rat anterior pituitary cells
Authors: IIJIMA T. , SAND O. , SEKIGUCHI T. , MATSUMOTO G.
Published: December 2008

The response to thyroliberin in prolactin‐producing rat GH4C1 clonal cells was studied using fura‐2 to monitor the cytosolic Ca2+ level ([Ca2+]i) in single cells, combined with recordings of membrane potential and current. The average value of [Ca2+]i was 109 nM (mean±SD, n= 112), and evoked action potentials caused transient elevations of about 100 nM. At higher firing frequencies these transients merged to a sustained elevation. In 100 % of the cells thyroliberin caused an instant rise in [Ca2+]i, peaking at 795±300 nM (n= 112). This first phase of the thyroliberin response was associated with hyperpolarization in current clamp and outward current in voltage clamp, caused by the opening of Ca2+‐activated K+ channels. In 75 % of the cells the initial peak in [Ca2+]i was followed by a prolonged plateau phase at 247±76 nM (n= 84). In current clamp the second‐phase elevation of [Ca2+]i was linked to either a modest depolarization in combination with enhanced firing frequency or a more pronounced depolarization in silent cells. This elevation of [Ca2+]i was reversed by hyperpolarizing current injection. No second‐phase elevation of [Ca2+]i was observed during voltage clamp at a holding potential of ‐ 50 mV. Short exposure to Ca2+‐free conditions eliminated the second‐phase elevation in [Ca2+]i, whereas the first phase remained intact. Our experiments show a direct relationship between electrical activity and [Ca2+]i in the GH4C1 cells. The second‐phase elevation of [Ca2+]i caused by thyroliberin is the result of influx through voltage‐sensitive Ca2+ channels, without involving agonist‐gated channels.
Testosterone elevates pituitary prolactin content of long‐term castrated rats under constant but not under periodic light
Authors: PORKKA‐HEISKANEN T. , LAAKSO M.‐L. , STENBERG D. , PEDER M. , JOHANSSON G.
Published: December 2008

Intact and castrated male rats were kept for 1 week under constant or periodic light, during which time they received daily injections of either vehicle or testosterone propionate (125 or 250 μg day‐1). Immediately after the experiment the rats were decapitated and serum and pituitary prolactin were measured radioimmunologically. The pituitary prolactin content was decreased after castration in both lighting conditions. Daily testosterone injections elevated the pituitary prolactin content of the castrated rats to the level of the intact rats in constant‐light conditions but were ineffective under periodic light. Serum prolactin concentrations were not affected by constant light.

We have previously shown that testosterone decreases the serum luteinizing hormone concentration of castrated rats more effectively under constant than under periodic light. In the present study we showed that serum prolactin was not elevated in constant light and thus could not be the cause of increased testosterone sensitivity. We also showed that testosterone elevates the pituitary prolactin content of castrated rats under constant but not under periodic light. This finding gives further support to the hypothesis that constant light sensitizes the hypothalamo‐pituitary axis of castrated male rats to the effects of testosterone.
Role of endothelium‐derived nitric oxide in the regulation of tonus in large‐bore arterial resistance vessels, arterioles and veins in cat skeletal muscle
Authors: EKELUND U. , MELLANDER S.
Published: December 2008

The role of endothelium‐derived nitric oxide in the regulation of vascular resistance (tonus) in cat skeletal muscle was studied with the use of NG‐monomethyl‐l‐arginine (L‐NMMA), a specific inhibitor of nitric oxide formation from l‐arginine. The study was performed with a whole‐organ technique which permits simultaneous, continuous and quantitative recordings of resistance reactions in the whole vascular bed (Rt/Sb>) and in its three consecutive sections: large‐bore arterial resistance vessels (>25 μm; Ra. prox) small arterioles (< 25 μm; Ra, miero) and veins (Rv. NG‐monomethyl‐L‐arginine (3–100 mg kg‐1 tissue, i.a.) induced a dose‐dependent increase in resistance that was preferentially, but not selectively, confined to the large‐bore arterial resistance vessels. At a maximally effective dose (100 mg kg‐l), the nitric oxide inhibitor caused a marked constriction, within 5 min, on average increasing Rt by 99%, Ra, prox by 138%, Ra, miero by 18% and Rv by 23%. The constrictor response to Ng‐monomethyl‐L‐arginine was long‐lasting but disappeared gradually over a period of about 1 h. However, it could be abruptly abolished by excess L‐arginine (300 mg kg‐1, i.a.). The vasodilator response (Rt) to acetylcholine was significantly attenuated in the presence of N'‐monomethyl‐L‐arginine compared with the control response. The results suggested that nitric oxide formation from L‐arginine by the vascular endothelium plays a fundamental role in the regulation of vascular resistance (tone) in vivo, with its main site of action located in the large‐bore arterial resistance vessels.
Biochemical and histochemical adaptation to sprint training in young athletes
Authors: CADEFAU J. , CASADEMONT J. , GRAU J. M. , FERNÁNDEZ J. , BALAGUER A. , VERNET M. , CUSSÓ R. , URBANO‐MÁRQUEZ A.
Published: December 2008

The purpose of the present study was to investigate the effects of 8 months of a specific and controlled sprint training programme on three groups of young athletes (two groups of males and one of females). Biopsies of vastus lateralis were taken before and after the period of training. The type percentage and diameter of the fibres, as well as the glycogen content and the activities of the enzymes of glycogen metabolism (glycogen synthase and glycogen phosphorylase), glycolysis (phosphofructokinase, pyruvate kinase, aldolase and lactate dehydrogenase), oxidative metabolism (succinate de‐hydrogenase) and creatine kinase and aminotransferases were studied. The results show an increase in the percentage of type I fibres and an increase in the diameter of both fibre types. A significant increase was also observed in glycogen content, and in the activities of glycogen synthase, glycogen phosphorylase, phosphofructokinase, pyruvate kinase, succinate dehydrogenase, aspartate aminotransferase and alanine aminotransferase. We conclude that a long period of sprint training induces a biochemical muscle adaptation to anaerobic exercise. This metabolic adaptation is followed by a morphological adaptation, although this is probably not as specific as the biochemical one.
The distribution of blood flow and glucose uptake within single skeletal muscles in the awake rabbit
Authors: IVERSEN P. O. , NICOLAYSEN G.
Published: December 2008

We have previously described a substantial regional heterogeneity both in blood flow and in glucose uptake within single skeletal muscles in anaesthetized rabbits. These heterogeneities could be related to effects of anaesthesia. The main goal of the present study was therefore to study regional muscle blood flow and muscle glucose uptake in awake rabbits.

We used the microsphere method and the deoxyglucose technique for assessment of regional blood flow and regional glucose uptake respectively. The measurements were performed in 0.25‐g regions from hind leg muscles. Some rabbits were first studied while awake and then during anaesthesia. Others were studied while either awake or anaesthetized.

The degree of regional heterogeneity in blood flow and in glucose uptake was similar in awake and anaesthetized rabbits. Both temporal and spatial heterogeneity in blood flow were present. Evidence was found for vasomotion with a cycle time exceeding 45 min in awake rabbits. This perfusion pattern was similar in rabbits in which either the motor or sympathetic vasomotor nerves or both had been blocked.

We conclude that regional perfusion and glucose uptake within single muscles are also markedly heterogeneous in awake rabbits. Regional, non‐synchronized fluctuations in blood flow with a long cycle time seem to be an important part of this perfusion heterogeneity.
Occurrence of phospholipase A2 and lysophospholipase in a gastric H, K‐ATPase‐containing membrane fraction, and the formation of lysophosphatidylcholine in stimulated pig parietal cells
Authors: OLAISSON H. , ARVIDSON G. , MA J.‐Y. , MÅRDH S.
Published: December 2008

A membrane fraction containing ‐ATPase (EC 3.6.1.36) was prepared from pig gastric mucosa and found to contain phospholipase A, (EC 3.1.1.4) and lysophospholipase (EC 3.1.1.5) activities. Washing the membranes decreased their protein content by 25%. Recovery profiles of ‐ATPase, phospholipase A, and lysophospholipase were similar for membranes washed either with water or with 0.15 or 1.5 m KCI. Nearly identical distribution profiles were obtained for the three enzyme activities after centrifugation of washed vesicle membranes on a linear sucrose gradient. The phospholipase A2 activity was stimulated by calcium and increased further in the presence of calmodulin.

The amount of cellular radioactively labelled lysophosphatidylcholine was doubled upon cholinergic stimulation of isolated parietal cells prelabelled with [3H]glycerol or 32P1. The liberated lyso(32P]phosphatidylcholine had its acyl chain in the sn‐1 position, which implies an activation of a phospholipase A2. These findings indicate that secretagogues which increase the cytosolic Ca2+ concentration, i.e. acetylcholine, histamine and gastrin, may activate a phospholipase A2 in the parietal cell.
Calcium and calmodulin stimulate phospholipase A2 and fusion of ‐ATPase‐containing membrane vesicles isolated from pig gastric mucosa
Authors: OLAISSON H. , MÅRDH S. , ARVIDSON G.
Published: December 2008

Fusion of pig gastric ‐ATPase‐ and phospholipase A,‐containing vesicles in vitro was studied by electron microscopy and by monitoring the change in fluorescence of octadecyl rhodamine B‐labelled vesicles. Ca2+ stimulated fusion of the vesicles, and the fusion rate showed a positive correlation with the activity of the phospholipase A2. Both the Ca2+‐stimulated fusion rate and the Ca2+‐dependent phospholipase A2 activity were further enhanced by the presence of calmodulin. The present results supported our previous findings (Olaisson et al. 1990) and further indicate that the phospholipase A2 associated with the ‐ATPase‐containing membranes might play a central role in membrane fusion processes in the stimulated parietal cell.
Reversible increase in light scattering during recovery from fatigue in Xenopus muscle fibres
Authors: WESTERBLAD H. , LÄNNERGREN J.
Published: December 2008

During recovery from fatigue produced by repeated tetanic stimulation, isolated Xenopus muscle fibres often enter a reversible state of severely depressed tension production. This post‐contractile depression has previously been found to be accompanied by an altered light microscopical appearance of fibres (increased light scattering), which suggests some morphological change as the cause of the force reduction. In the present study the relation between tension production and light scattering (measured as optical density) has been studied in more detail. It was found that fibres developing a marked post‐contractile depression exhibited the largest increase in light scattering. When fibres recovered from post‐contractile depression, an increased optical density remained in the central region of fibres, and this region also produced less tension. The tension output of fibres recovering without post‐contractile depression declined markedly when the tonicity of the bathing solution was raised, and this decline was accompanied by increased optical density. However, a close temporal correlation between increased light scattering and tension depression was not always found: in some fibres the time course of changes in light scattering differed from that of the tension depression.

In summary, the present results show that reversible structural changes may develop after fatiguing stimulation, and some form of coupling between these changes and the force depression during post‐contractile depression is suggested.
Striatal dopamine and glutamate release: effects of intranigral injections of substance P
Authors: REID M. S. , HERRERA‐MARSCHITZ M. , KEHR J. , UNGERSTEDT U.
Published: December 2008

The levels of extracellular striatal dopamine and glutamate were measured simultaneously in halothane‐anaesthetized rats using microdialysis. Unilateral injections of substance P (0.07 nmol) into the substantia nigra, pars reticulata enhanced the levels of dopamine and glutamate in the ipsilateral striatum. Intranigral injections of neurokinin A (0.09 nmol) enhanced the levels of striatal dopamine, and intranigral injections of γ‐aminobutyric acid (300 nmol) or dynorphin A (0.5 nmol) decreased the levels of striatal dopamine, but none of these had any effect on the levels of striatal glutamate. Local perfusion with the dopamine agonists apomorphine (D1/D2), SKF 38393 (DI) or pergolide (D2) (each at 10‐5M)decreased the levels of striatal dopamine and enhanced the levels of striatal glutamate. In unilateral 6‐hydroxydopamine‐lesioned rats, basal striatal glutamate levels were decreased bilaterally. Furthermore, on the denervated side intranigral substance P stimulation of striatal glutamate levels was enhanced, while on the intact side intranigral substance P stimulation of striatal dopamine and glutamate levels was similar to that seen in normal rats. These findings suggest that striatonigral substance P provides a stimulatory regulation of ipsilateral striatal glutamate release. Furthermore, it is indicated that striatal glutamate release can also be regulated by dopamine terminals.
Further studies of the changes in alkaline secretion, transepithelial potential difference and net fluid transport induced by the heat‐stable enterotoxin of Escherichia coli (STa) in the rat jejunum in vivo
Authors: TANTISIRA M. H. , JODAL M. , LUNDGREN O.
Published: December 2008

A pH‐stat technique was used to study the mechanisms underlying the intestinal alkalinization evoked by the heat‐stable enterotoxin of Escherichia coli (STa) in the rat denervated jejunum in vivo. In addition, concomitant changes of transepithelial potential difference and fluid transport were also investigated. To test the possible involvement of the enteric nervous system in the ST,‐stimulated alkaline secretion and potential difference, the mesenteric nerves were electrically stimulated or neuropeptide Y or methionine‐enkephalin was infused intravenously. None of these interventions inhibited to any large extent the STa,‐stimulated alkaline secretion, whereas a greater suppression was noted on the concomitantly increased potential difference. Furthermore, neuropeptide Y but not methionine‐enkephalin significantly inhibited STa,‐induced jejunal fluid secretion although neuropeptide Y was without effect on basal fluid transport. It is concluded that the enteric nervous reflex(es) which are of significant importance in explaining ST,‐evoked fluid secretion plays a minor role in controlling alkaline secretion. Furthermore, alkaline secretion may not contribute to the increase in potential difference caused by ST., Amiloride (10‐4 or 1‐3 M) had no effect on the STa,‐stimulated alkaline secretion, implying that some cellular mechanism other than an inhibition of Na+/H+ exchanger explains the observed response. Similarly, acetazo‐lamide had no effect on the STa,‐stimulated alkaline secretion or potential difference, suggesting that the secreted alkaline is of extracellular origin rather than from the cellular metabolism in the enterocytes.
A continuous‐flow technique for analysis of stoichiometry and transport kinetics of gastric H, K‐ATPase
Authors: NORBERG L. , MÅDH S.
Published: December 2008

A continuous‐flow method was developed for determining the stoichiometry of the gastric proton pump H, K‐ATPase (EC 3.6.1.36) in its hydrolysis of ATP and translocation of H+ and the K+ congener “Rb+. H, K‐ATPase‐containing vesicles which had been isolated from pig gastric mucosa were incubated at 37 °C for 2 h in 150 mM 86RbCl, 0.5 mM ethylenebis(oxyethylenenitrilo)tetra‐acetic acid and J mM 2–(N‐morpholino)ethane sulphonic acid (Mes) adjusted to pH 6.1 with Tris, and then applied onto a 0.45 μm pore size cellulose acetate filter. The immobilized vesicles were perfused with 0.15 mM Mes/Tris buffer, pH 6.1, containing 150 mcholine chloride and 0.2 mM MgCl2., After changing to a medium containing 0.1 mM ATP, the amounts and rates of H+ uptake, 86Rb+ efflux and ATP hydrolysis were measured. The initial ratio of Rb+ transported to ATP hydrolysed gave values of 0.96 ± 0.26 (mean f SD, n= 28). The initial ratio of ATP‐dependent Rb+ efflux to H+ uptake gave values of 0.92 + 0.28 (mean f SD, n= 28). The Mg‐ATPase activity was measured in vesicles which had been incubated with choline chloride instead of RbC1. This activity was 15.8 f 8.7% (mean + SD) of the total ATPase activity in the initial fractions used for calculation of the stoichiometry. It is argued that this Mg‐ATPase may be an intrinsic activity of the H, K‐ATPase and that the relation between these activities is dependent on the amount of K+ (or Rb+) present in the assay. However, whether corrections were made for this Mg‐ATPase or not, it had only marginal effects on the calculations of the stoichiometry of the pump. Thus simultaneous measurements of 86Rb+ efflux, H+ uptake and ATP hydrolysis in immobilized gastric vesicles gave a stoichiometry of the pump close to a 1:1:1 ratio. These results indicate that the pump is non‐electrogenic.
Daily patterns of plasma atrial natriuretic peptide, serum osmolality and haematocirt in the rat
Authors: KANERVO A. , ARJAMAA O. , VUOLTEENAHO O. , LEPPÄLUOTO J.
Published: December 2008

The present study documents daily rhythms of plasma atrial natriuretic peptide, serum osmolality and haematocrit in the rat. One‐hundred and twenty‐five Sprague‐Dawley rats were used. They were bred under a cycle of 12 h light/12 h dark starting at 07.00 h. Fifty‐three rats were decapitated between 09.00 and 16.00 h (study I) and 72 rats in groups of six were decapitated at 2‐h intervals for a period of 24 h (study II). In study I, plasma atrial natriuretic peptide was 156±11 pg mg‐1 (mean ± SEM). In study II, atrial natriuretic peptide was at a control level from 08.00 to 18.00 h and then began to increase. At 22.00 h, atrial nartriuretic peptide was 420 ± 105 pg ml‐1, which was significantly higher than at 08.00 h (P < 0.05). The serum osmolality was over 300 mosmol kg‐1 during the day. The highest mean osmolalities (315, 317, 312 mosmol kg‐1 were found from 18.00 to 22.00 h. These were significantly different (P < 0.05) from other groups during the day. The haematocrit was highest at 14.00 h (49.5 ± 0.7%) and lowest at 24.00 h (43.6 ± 0.8%) (P < 0.05).

In conclusion, we have shown that there are significant daily rhythms of plasma atrial natriuretic peptide, serum osmolality and haematocrit during a 24‐h period and 12 h light/12 h dark cycle in the rat.
Nitric oxide requirement for vasomotor nerve‐induced vasodilation and modulation of resting blood flow in muscle microcirculation
Authors: PERSSON M. G. , WIKLUND N. P. , GUSTAFSSON L. E.
Published: December 2008

Intravital microscopy of rabbit tenuissimus muscle was used for studies of endogenous nitric oxide as a microvascular regulatorin vivo.Derivatives of were administered in order to modulate the formation of nitric oxide from L‐arginine. Nw‐nitro‐L‐arginine methylester (L‐NAME) (1‐100 mg kg‐1i.v.) dose‐dependently reduced microvascular diameters. A concomitant blood pressure increase and a decrease in heart rate was observed. The blood pressure increase induced by L‐NAME (30 mg kg‐1) was reversed by L‐arginine (1 g kg‐1) but not D‐arginine. Vasodilation in response to topical acetylcholine (0.03‐3 μM) was significantly inhibited by L‐NAME (30 mg kg‐l), whereas vasodilation by sodium nitroprusside (300 nM) was not affected. Vasomotor nerveinduced vasodilatation, induced by stimulation of the tenuissimus nerve after neuromuscular blockade by pancuronium in animals pretreated with guanethidine, was significantly attenuated by L‐NAME, an effect also reversed by L‐arginine. The vasodilatation in response to active contractions of the muscle induced by motor nerve stimulation as well as the vasodilator response elicited by graded perfusion pressure reductions were unaffected by L‐NAME or NG‐monomethyl‐L‐arginine (L‐NMMA, 10‐4M) administered topically.

Our results indicate that endogenous nitric oxide formed from L‐arginine is a modulator of microvascular tonein vivo.Furthermore, the results suggest that endogenous nitric oxide is required for vasomotor nerve‐induced vasodilatation, whereas it does not appear to play a role in myogenic vasodilatation or functional hyperaemia in this tissue.
Evidence for a link between mechanical and electrical alternans in acutely ischaemic myocardium of anaesthetized dogs
Authors: HASHIMOTO H. , NAKASHIMA M.
Published: December 2008

In order to examine the relation between mechanical alternans and associated electrical alternans during acute myocardial ischaemia, we determined the effect of a ventricular premature beat and calcium antagonists on mechanical and electrical alternans during acute coronary occlusion in anaesthetized dogs. Isometric contractions and unipolar electrocardiograms were recorded from ischaemic myocardium. During coronary occlusion, mechanical alternans was accompanied by electrical alternans, which was an alternate change in the ST segment elevation, i.e. the higher ST and the lower ST. Electrical alternans was frequently discordant and in some cases accompanied by discordant mechanical alternans. Both discordant electrical and mechanical alternans became concordant and were potentiated after the ventricular premature beat. In all cases, concordant mechanical alternans was accompanied by concordant electrical alternans and vice versa. In this situation, the higher and the lower ST corresponded to the larger and the smaller contractions respectively. Thus, a fixed correspondence was observed between mechanical and electrical alternans. A fixed correspondence was also observed between mechanical alternans and the variation in the time taken for repolarization of the monophasic action potential. Verapamil and diltiazem inhibited both electrical and mechanical alternans. The present results support the idea that a common mechanism, such as a beat‐to‐beat cycle of the transmembrane and intracellular movement of calcium ions, may play a role in the mechanisms of electrical and mechanical alternans.
Characteristics of ascorbic acid uptake by isolated ox neurohypophyseal nerve terminals and the influence of glucocorticoid and tri‐iodothyronine on uptake
Authors: THORN N. A. , NIELSEN F. S. , JEPPESEN C. K.
Published: December 2008

Isolated nerve endings (neurosecretosomes) from ox neurohypophyses took up L‐[14C]ascorbic acid by a process or processes which showed energy dependence and which could be inhibited by unlabelled ascorbic acid in micromolar concentrations and by isoascorbic acid in millimolar concentrations, whereas dehydroascorbic acid only inhibited in concentrations of about 100 mM. The uptake showed saturation with increasing concentration of ascorbic acid and a Km value of 97 μ Uptake was inhibited by increasing glucose concentration in the medium or by adding cytochalasin B, phloridzin, ethanol or probenecid to the medium. The uptake was inhibited by lowering the sodium concentration and by lack of calcium. These facts suggest the presence of both a glucose‐dependent uptake and a sodium‐dependent uptake. Cortisol and triiodothyronine inhibited uptake. This effect of cortisol, but not of tri‐iodothyronine, was dependent on the presence of sodium in the medium. For both hormones it was still present when phloridzin or probenecid was added to the medium.
Production of transferable neuronotrophic factor(s) by human midgut carcinoid tumours cells; studies using cultures of rat fetal choloinergic neurons
Authors: WIGANDER A. , LUNDMARK K. , McRAE* A. , MÖLNE J. , NILSSON O. , HAGLID K. , DAHLSTRÖM A. , AHLMAN H.
Published: December 2008

A co‐culture system was established between human midgut carcinoid tumour cells and rat fetal cholinergic neurons. In monocultures in serum‐free media, only tumour cells survived, while neurons deteriorated. In serum‐free co‐cultures, neurons displayed outgrowth of neuritic processes. Neurons of neuronal serum‐free monocultures thrived if supplemented with conditioned media from tumour cell cultures grown serum‐free. This indicates that tumour cells produce transferable growth factor(s) with potent neuronotrophic actions. Immunocytochemical studies indicate that this growth factor resembles nerve growth factor immunologically, since tumour cells were strongly immunoreactive after incubation with a rabbit anti‐nerve growth factor antiserum, and furthermore expressed immunoreactive nerve growth factor receptors.
Lithium absorption by the rabbit gall‐bladder
Authors: HANSEN C.P. , HOLSTEIN‐RATHLOU N.‐H. , SKØTT O. , LEYSSAC P.P. , FREDERIKSEN O.
Published: December 2008

Lithium (Li+) absorption across the low‐resistance epithelium of the rabbit gall‐bladder was studied in order to elucidate possible routes and mechanisms of Li+ transfer. Li+ at a concentration of 0.4 mM in both mucosal and serosal media did not affect isosmotic mucosa‐to‐serosa fluid absorption. At this low concentration net mucosa‐to‐serosa Li+ absorption was insignificant when the ambient Na+ concentration was 115 mM, although the gall‐bladder had a significant Li+ permeability (2.7 times 10‐5 cm‐1) and a significant mucosa‐to‐serosa Li+ gradient developed as a result of fluid absorption. Net Li+ absorption was induced at reduced mucosal Na+ concentrations (by lowering the Na+ concentration down to 50 mM with or without substitution with sucrose, or by adding sucrose to the mucosal medium). This Li+ absorption occurred even in the absence of a mucosa‐to‐serosa Li+ gradient. Na+ and Li+ absorptions occurring at 50 mM Na+ were inhibited to the same degree by mucosal 1 mM amiloride. Substitution of 5–50 mM (44%) Na+ by Li+ in the external medium dose‐dependently depressed Na+ absorption by up to 76%, while substitution by 50 mM choline had no significant effect. Li+ inhibition of Na+ absorption was elicited from the mucosal side and was not accounted for by compensatory Li+ absorption; water and Na+ absorption rates decreased nearly in parallel. The effects of 0.4 mM amiloride and of substitution with 20 mM Li+ were only partly additive. It is concluded that Li+ absorption in the rabbit gall‐bladder cannot be explained by passive (paracellular) transport, but must be the result of transcellular, active transport. Both at low and at high concentrations Li+ may enter the cell via an Na+/H+ exchanger in the apical cell membrane. At high concentrations Li+ may inhibit Na+ absorption by interference with the exchange mechanism and/or via effects at the cytoplasmic level. The Li+ transfer mechanism across the basolateral cell membrane remains unknown.
On the non‐adrenergic, non‐cholinergic contribution to the parasympathetic nerve‐evoked secretion of parotid saliva in the rat
Authors: MÅNSSON B. , EKSTRÖM J.
Published: December 2008

A secretion of parotid saliva in the anaesthetized rat in response to stimulation of the parasympathetic nerve occurs in the presence of atropine and adrenoceptor antagonists, albeit reduced and transient in the face of continuous high‐frequency stimulation (40 Hz). In non‐atropinized rats prolonged stimulation of the parasympathetic nerve at a high frequency (40 Hz, 40 min), aiming at depletion of the neuronal stores of transmitters thought to be responsible for the non‐adrenergic, non‐cholinergic (NANC) secretion of parotid saliva, was performed. The magnitude of the secretory response to various stimulation frequencies (0.2–60 Hz) applied to the parasympathetic nerve was assessed before and after the period of high‐frequency stimulation. The second time, the frequency‐response curve was shifted to the right and, moreover, the initial maximal secretory response was not reached. Control experiments suggested that this reduction in secretory responses could be attributed neither to impaired cholinergic neurotransmission nor to decreased responsiveness of the secretory cells. The secretory responses to parasympathetic nerve stimulation after high‐frequency stimulation are thought to be evoked by acetylcholine predominantly. When these responses were compared with (1) those obtained before high‐frequency stimulation and thought to be evoked by acetylcholine and non‐adrenergic, non‐cholinergic transmitters in conjunction and (2) those depending on non‐adrenergic, non‐cholinergic transmitters only it appears that the non‐adrenergic, non‐cholinergic transmission contributes to the parasympathetic secretory response at a frequency (0.2 Hz) far below threshold frequency (5 Hz) for the non adrenergic, non‐cholinergic evoked secretory response. At frequencies below 20 Hz it appears that acetylcholine and non‐adrenergic, non‐cholinergic transmitters interact positively thereby enhancing the secretory responses.
Secretin dissipates red aridine orange fluoescence from pancreatic duct epithelium
Authors: VEEL T. , BUANES T. , GROTMOL T. , ØTENSEN J. , ÆDER M. G. R.
Published: December 2008

This study was undertaken to elucidate whether duct cells in the pancreas contain acidic cytoplasmic compartments regulated by secretion. Microdissected pancreatic ducts from pigs were examined by acridibe orange (AO) and 2′, 7′‐biscarboxyethyl‐5(6)‐carboxyfluorescein/tetraacetioxymethyl ester (BCECF/AM) epifluorescence microscopy. Estimated cytoplasmic pH using BCECF fluorescence was 7.43pL0.04 and was not changed by altering CO2 tension in the incubation mdium. The epithelium of acridine orange incbated peripheral interlobular pancreatic ducts exhibited green and fluorescence was sen in resting pancreatic ducts and was greatly accentuated by raising CO2 in the incubation medium with chloroqyuine or NH4Cl or the protonophores carbonyl cyanide p‐trifluoromethoxyphenylhydrazone (FCCP) or carbonyl cyanide M‐chlorophenylhydrazone (CCCP), leaving uniform gren fluoresence. These findings suggest that pancreatic duct cells contain CO2‐dependent acidic compartments which vanishduring seceatin stimulation and which may be cytoplasmic tubulovesicles.
Plasma atrial natriuretic peptide and vasopressin during thermal dehydration in supine posture
Authors: MELIN B. , CURÉ M. , JIMENEZ C. , ALLEVARD A. M. , GEELEN G. , GHARIB C.
Published: December 2008

After 30 minutes spent in an upright posture six healthy male subjects underwent two 130‐minute experiments in a supine posture, the first in thermoneutral conditions (TC) and the second, 15 days later, in a hot environment (HE) in order to obtain a water loss of 2.5%) body weight. In thermoneutral conditions, the supine posture induced plasma volume expansion, resulting in slightly lowered plasma vasopressin (AVP) levels and higher plasma atrial natriuretic peptide (ANP) levels, compared to the values obtained in the upright posture (P < 0.05). During hot environment, the sweating‐induced dehydration led to a significant reduction of plasma volume expansion and to an increase in rectal temperature and plasma osmolality (P < 0.05). Plasma vasopressin levels were higher at the end of the heat exposure (P < 0.05) but natriuretic peptide levels did not change, compared to the values observed in the upright posture. These data suggest that plasma volume reduction induced by thermal dehydration may limit the natriuretic peptide release, which occurs after changing from the upright to a supine position.
Diurnal variations in central venous pressure
Authors: ENGEL B.T. , TALAN M.I.
Published: December 2008

We analysed the haemodynamic patterns of seven monkeys (Macaca mulatta) during a one‐month period during which we monitored beat‐to‐beat levels of heart rate, stroke volume, intra‐arterial pressure and central venous pressure 7 days/week, 18 h/day. We replicated an earlier finding that cardiac output falls and total peripheral resistance rises throughout the night: the fall in cardiac output was mediated by a fall in heart rate since stroke volume did not change; and the rise in peripheral resistance reflected a homeostatic adjustment to the fall in cardiac output since blood pressure was stable throughout the night although it fell early in the evening. In addition, we have shown for the first time that central venous pressure also falls throughout the night; this occurs even in the presence of α‐and β‐adrenergic sympathetic blockade. Since stroke volume does not change overnight this indicates that the nocturnal fall in cardiac output is not due to a shift of blood volume into the venous compartment. These findings support our hypothesis that there is a nocturnal decline in plasma volume.
Dual response from human muscle spindles in fast voluntary movements
Authors: AL‐FALAHE N. A. , NAGAOKA M. , VALLBO A. B.
Published: December 2008

Single‐unit impulses were recorded from the radial nerve of attending human subjects using the microneurography technique. The discharge of muscle spindle afferents from the extensor digitorum muscles was analysed while subjects performed fast lengthening and shortening voluntary movements as well as movements of moderate speed at a single metacarpophalangeal joint. Opposing or assisting loads of moderate size were added in some tests.

Fast lengthening movements were, in practically all units, associated with acceleration of spindle discharge. However, the responses were modest and in many primary afferents it was of similar size as their response to small irregularities during slower movements.

During shortening movements, most spindle afferents stopped firing altogether, whereas some afferents exhibited a distinct burst of impulses at the onset of active shortening followed by silence during the main part of the movement. This initial shortening responses was sometimes more prominent when the parent muscle worked against an opposing load. It was interpreted as a result of fusimotor drive associated with the building up of force in the contracting muscle.

The initial shortening response from the contracting muscle and the stretch response from the antagonist constitute a dual signal, describing accurately the onset of joint movement as seen from the two muscles. It remains to be clarified which role this pattern of afferent responses may have in the design of the current motor output and in the capturing of nature and size of the external load.
Stimulation of airway ciliary motility by immunologically activated canine pulmonary macrophages: role of leukotrienes
Authors: TAMAOKI J. , SAKAI N. , KOBAYASHI K. , KANEMURA T. , TAKIZAWA T.
Published: December 2008

To elucidate a possible interaction between alveolar macrophages and airway epithelial cells in allergic conditions, we studied the effect of immunologically stimulated macrophages on ciliary beat frequency (CBF) of cultured canine tracheal epithelium by a photoelectric method. Administration of supernatants from macrophages incubated with anti‐dinitrophenyl (DNP) IgE antibody and anti‐dinitrophenyl‐human serum albumin dose‐dependently increased ciliary beat frequency, the maximal increase from the baseline being 30.4 pL 5.0% (mean pL SE, P0.01), an effect that was accompanied by the release of leukotriene (LT) C4 and leukotriene D4. This ciliostimulation was not affected by pretreatment of macrophages with indomethacin but was inhibited by that with nordihydroguaiaretic acid. Addition of FPL 55712 abolished the response of ciliary beat frequency to the stimulated macrophages, and exogenously administered leukotriene C4 and leukotriene D4 dose‐dependently increased ciliary beat frequency. These results suggest that macrophages increase respiratory ciliary motility through the IgE‐mediated release of leukotrienes and may modulate mucociliary transport function in the airway.
Mechanism of anoxic conduction block in mammalian nerve
Authors: LINDSTRÖM P. , BRISMAR T.
Published: December 2008

The mechanism by which anoxia blocks impulse conduction was studied in isolated sciatic nerves from the rat. The desheathed nerve was mounted in a recording chamber, and the compound action potential (CAP) was measured at controlled temperature (23 and 37 d̀C). When the nerve was irrigated with nitrogenated Ringer's solution compound action potential decreased to 50% in 10 min at 37 d̀C and in 35 min at 23 d̀C, whereas in oxygenated solution compound action potential decreased less than 5% in 60 min. A Na‐free nitrogenated solution similarly caused anoxic block, that is the effect was independent of impulse activity. Ouabain (1 mm) decreased compound action potential by only ca. 4% in 30 min, and the effect of anoxia was delayed in presence of ouabain. Dinitrophenol (0.05 mm) reduced compound action potential to 50% in 5 min. These findings indicated that the anoxic block was not related to changes in axonal concentration of Na or K following impulse activity or inhibition of Na‐K‐ATPase. Instead the findings imply that the anoxic block is due to inactivation of Na‐channels as a consequence of inhibition of another ATP‐dependent process in the axon.
Is the humoral renal antihypertensive activity of the spontaneously hypertensive rat (SHR) reset to the high blood pressure?
Authors: Karlström G. , Bergström G. , Folkow B. , Rudenstam J. , Göthberg G.
Published: December 2008

The kidneys have a humoral antihypertensive system, located in the renal medulla and presumably antagonizing the pro‐hypertensive renin‐angiotensin system. Medullipin I and II and maybe platelet activating factor (PAF), seem to be the mediators of this system, known to be activated after reversal of renovascular hypertension or when the perfusion pressure to a normotensive kidney is suddenly elevated.

The present study was undertaken to investigate whether this system is functioning also in the spontaneously hypertensive rat (SHR), and if it is then reset in proportion to the increased mean arterial pressure (MAP). Isolated kidneys from spontaneously hypertensive rats and from Wistar Kyoto rats (WKY) were cross‐perfused in vivo from anaesthetized intact Wistar Kyoto rat ‘donors’. After 30 min of perfusion at 100 mmHg the perfusion pressure to the isolated kidneys were, for 60 min, either kept unaltered at 100 mmHg or, for the Wistar Kyoto rat kidneys, increased to 150–200 mmHg and, for the spontaneously hypertensive rat kidneys, raised to 200 or 250 mmHg.

The results show that the humoral antihypertensive system is present also in spontaneously hypertensive rat kidneys, but is here reset upwards to or even beyond the elevated MAP level. Furthermore, all mean arterial pressure reductions caused by high‐pressure perfusion of Wistar Kyoto and spontaneously hypertensive rat kidneys were accompanied by reductions in heart rate (HR) in the ‘donors’, in agreement with previous observations after reversing renal hypertension and after i.v. medullipin I injection.

In fact, in spontaneously hypertensive rat kidneys, the ‘incretory’ depressor mechanism appears to be more markedly reset upwards than is the ‘excretory’ depressor mechanism inherent in pressure diuresis with consequent salt‐volume elimination.

In conclusion spontaneously hypertensive rats, like Wistar Kyoto rats and Wistar rats, have a humoral antihypertensive system in the kidneys, but it is reset upwards even beyond the elevated mean arterial pressure level in spontaneously hypertensive rats. The combination of a depressor response and reduced heart rate in the ‘donors’ renders further evidence that the medullipins are the principal, though probably not the only, humoral antihypertensive factors released from the cross‐circulated kidneys.