bluuebunny/crossref_metadata_2025 huggingface dataset:
Ammonium chloride induced acidosis and aldosterone secretion in the goat
Authors: AUGUSTINSSON O. , JOHANSSON K.
Published: December 2008

Responses to 30‐min intraduodenal infusion of NH4Cl (total amount 75 mmol) were studied in conscious goats. The infusion caused an immediate, transient rise in plasma aldosterone concentration (PA) from a mean of 78 to 221 pmo l‐1. As expected, the NH4Cl administration also induced metabolic acidosis, initially subjected to partial respiratory compensation. The acidosis did not become fully developed until 1 h after cessation of the infusion, when PA had almost returned to its initial level. Renal compensation of the acidosis was shown by acidification of the urine and reduced Na excretion being most pronounced 1–2 h post‐infusion. During the infusion blood haemoglobin concentration and the haematocrit increased by 25 and 13%, respectively, without simultaneous increase in plasma protein concentration and with persisting ear vasodilatation, indicating a mobilization of stored erythrocytes in the absence of a general increase in sympathetic tone. The results suggest that the reduction of blood pH is not the cause of the increase in PA occurring in association with NH4Cl‐induced metabolic acidosis, but leave open the possibility that this increase may be due to some centrally mediated or direct adrenal influence of NH4+. As regards the apparent NH4Cl‐induced mobilization of stored erythrocytes, it is suggested that such a response may play a role in the defence against acidosis by increasing the buffering capacity of the circulating blood.
Potassium and chloride fluxes are involved in volume regulation in mouse pancreatic islet cells
Authors: LINDSTRÖM P. , NORLUND L. , SEHLIN J.
Published: December 2008

Potassium and chloride transport were measured in β‐cell‐rich islets from ob/ob‐mice using 36Cl‐86Rb+ (K+‐analogue). Reduction of the osmolarity from the normal 317 mosm l‐1 to 180 mosm l‐1 reduced the apparent content of K+ Cl1. Hypo‐osmolarity had no effect on the ouabain‐sensitive portion of the Rb+ influx (Na+/K+ pump), but reduced the ouabain‐resistant portion of the influx. Hypo‐osmolarity also strongly increased the Rb+ efflux rate. Both tetracaine (0.5 mitt) and glibenclamide (20 μM), which increase the osmotic resistance of pancreatic β cells, significantly potentiated the reduction in apparent K+ content induced by hypo‐osmolarity. This study suggests that the volume regulation in pancreatic β cells is partly due to K+ Cl‐ flux and that glibenclamide and tetracaine increase the osmotic resistance of the β cells by affecting such ion transport.
Simultaneous measurements of gastric motility and acid‐bicarbonate secretions in the anaesthetized cat
Authors: FÄNDRIKS L. , STAGE L.
Published: December 2008

Chloralosed cats were acutely vagotomized, their splanchnic nerves cut and the adrenal glands ligated. The gastric lumen was perfused with isotonic NaCl and gastric motility was monitored as changes in hydrostatic pressure within the perfusion circuit. Gastric secretion of H+ HCO3‐ were calculated from continuous measurements of pH and Pco2 Methodological tests ex vivo showed good accuracy of the estimations. Recovery of H+ after HCl instillation into the stomach in vivo was almost complete, while HCO3‐ recovery after NaHCO3 instillatons was 85–95%. Pentagastrin (10μg kg‐1 h‐1 i.v.) stimulated gastric contractile activity and increased gastric H+ secretion 30‐fold, while HCO3‐ secretion decreased somewhat. Carbachol (4μg kg‐1 h‐1) induced gastric contractions and increased H+ secretion by 400% and HCO3‐ output by 100–130%. Electrical stimulation of the cut vagal nerves (10 Hz for 10 min) induced well known gastric motor responses and increased gastric H+ secretion 20‐fold preceded By a transient doubling of HCO3‐ secretion. Omeprazole, a selective inhibitor of gastric H+ secretion, decreased the vagally induced H+ secretion, while recorded gastric HCO3‐ secretion was clearly enhanced. In conclusion, the technique permits simultaneous recordings of rapid alterations of gastric motility and H+ HCO3‐ secretions. However, HCO3‐ secretion was modestly underestimated, probably due to mucosal CO2 absorption.
The effects of naloxone on cerebral function in spontaneously hypertensive rats during hypotensive haemorrhage
Authors: SKARPHEDINSSON J. O. , THORÉN PETER
Published: December 2008

The purpose of this study was to examine the effects of naloxone on signs of relative cerebral ischaemia induced by hypotensive haemorrhage. Mean arterial blood pressure (MAP), heart rate (HR), renal sympathetic nerve activity (rSNA) and somatosensory evoked potentials (SEP) were recorded in chloralose‐anaesthetized spontaneously hypertensive rats exposed to graded bleeding. Hypotensive haemorrhage resulted, after a very brief sympathetic excitation, in marked sympathetic inhibition and bradycardia and a considerable reduction of SEP, indicating relative cerebral ischaemia. However, after 25–30 min this sympatho‐inhibitory response was reversed to pronounced sympathetic excitation and tachycardia, which was accompanied by a further attenuation of SEP. A single bolus of naloxone (10 mg kg‐1) caused transient sympathetic inhibition and bradycardia, which was accompanied by an improvement of SEP. A bolus injection (5–10 mg kg‐1) followed by a 30 min infusion of naloxone (25–35 mg kg‐1 h‐I) caused a sustained SEP improvement despite the fact that MAP was kept constant during naloxone administration. We conclude that naloxone can have beneficial effects on brain function during cerebral ischaemia, effects that are probably due to blockade of opioid receptors. Our model of relative cerebral ischaemia might be useful for evaluating the mechanisms behind the naloxone effects during this condition.
Effects of the thromboxane‐receptor antagonist L‐636,499 on feline cerebral arteries
Authors: USKI T. K. , ANDERSSON K.‐E.
Published: December 2008

The effects of the thromboxane‐receptor antagonist L‐636,499 on contractions induced by U46619 and prostaglandin (PG)F2αwere studied in the isolated feline basilar artery (BA). L‐636,499 (10‐6‐3 times 10‐5mol l‐1) shifted concentration‐response curves induced by U46619 to the right in a parallel manner. By contrast, concentration‐response curves induced by PGF2αwere displaced only when L‐636,499 concentrations of 10‐53 times 10‐5mol l‐1were used. The Schild plot using U46619 as the agonist revealed a slope index (0.69) which was significantly less than unity.PA2‐values calculated according to the method of van Rossum differed significantly between different concentration intervals of L‐636,499. At 10‐6to 3 times 10‐6mol l‐1thePA2value was 5.99, whereas at 10‐5to 3 times 10‐5mol 1‐Iit was 5.59. Using PGF2αas the agonist thePA2‐value at the L‐636,499 concentration interval 10‐5to 3 times 10‐5mol 1‐Iwas 5.69. It may be concluded that the feline BA contains two receptor sites mediating prostanoid‐induced contraction, one of which may be characterized as a thromboxane‐sensitive (TP) receptor. L‐636,499 can interact with both receptor sites with highest affinity for the TP receptor site.
Force, relaxation and energy metabolism of rat soleus muscle during anaerobic contraction
Authors: SAHLIN K. , EDSTRÖM L. , SJÖHOLM H.
Published: December 2008

Isolated soleus muscle of rat was stimulated electrically (2 Hz) for 7 min under anaerobic conditions. Isometric twitch tension decreased progressively and was 30% of the initial value at the end of stimulation. The decline in relative force was similar to that previously observed in fast twitch muscle and soleus can thus not be termed fatigue‐resistant under anaerobic conditions. Phosphocreatine (PCr) decreased from (x̄± SD) 61.1 ± 4.4 at rest to 4.0 ± 1.8 mmol kg‐1 dry muscle (d.m.) after 7 min of stimulation, while lactate increased from 3.7 ± 1.6 to 30 ± 8 mmol kg‐1 d.m. Energy was thus derived from complete utilization of PCr and a low rate of glycolysis resulting in an almost unchanged calculated intracellular pH. It is concluded that tension decline in soleus muscle is not due to decreased intracellular pH but is more related to the capacity to regenerate ATP at a sufficient rate. Contraction and relaxation time of the twitch remained practically constant during the stimulation period. In contrast prolonged activation of fast‐twitch muscle results in a slowing of the relaxation of the twitch (Sahlin et al. 1981) and it has been suggested that this is caused by the decrease of intracellular pH. The constancy of both relaxation time and calculated pH in the fatigued soleus muscle is consistent with the hypothesis that there is a connection between these two parameters. In contrast to the twitch, relaxation of tension after a tetanus was prolonged in soleus. Hence, it appears that the rate limiting step for relaxation is different for a twitch than for a tetanus in soleus.
How bicarbonate loading inhibits tubular reabsorption of NaCI in dog kidneys
Authors: ØSTENSEN J. , LANGBERG H. , KIIL F.
Published: December 2008

During continuous infusion of ethacrynic acid in dogs, changes in glomerular filtration rate (GFR) andPco2at constant plasma bicarbonate concentration (PHCO3) alter bicarbonate and chloride reabsorption in a ratio of 1: 2. This ratio did not apply whenPHCO3was raised by bicarbonate loading in 11 anaesthetized volume‐expanded dogs. A rise inPHCO3from 30 to 54 mM at constantPco2and GFR reduced sodium reabsorption during ethacrynic acid infusion from 3586 ± 725 to 2449 ± 403 μmol min‐1. Bicarbonate and chloride reabsorption were reduced in a ratio of 1: 10. When plasma pH was restored from 7.8 to 7.5 by raisingPco2, the inhibitory effect on chloride reabsorption was halved. At constant plasma pH 7.5 a rise inPHCO3from 20 to 30 mM reduced chloride reabsorption by 20%. A further 30% inhibition was caused by raisingPHCO3from 30 to 54 mM. Bicarbonate reabsorption was highest atPHCO354 suggesting a large capacity for bicarbonate reabsorption ifPHCO3is raised at constant plasma pH 7.5. Water and NaCI reabsorption remaining during ethacrynic acid infusion is almost equally inhibited by alkalosis and by an osmotic effect of unreabsorbed NaHCO3.
Ultrastructural observations on beaded α‐motoneuron dendrites
Authors: LAGERBÄCK P.‐Å. , ULFHAKE B.
Published: December 2008

Beaded dendrites of 1α‐motoneurons intracellularly labelled with horseradish peroxidase (HRP) were studied ultrastructurally in eight adult cats. For comparison, adjacent unlabelled beaded dendrites of unknown origin were also included in the study. Electron microscopy revealed no signs of degeneration or poor fixation according to common criteria. With the exception of the HRP‐reaction product no difference in structure was observed between labelled and unlabelled beaded dendrites. Both the beads and their interconnecting segments were postsynaptic to boutons of normal appearance containing spherical (S‐type boutons) or flattened vesicles (F‐type boutons). The values for synaptic covering and synaptic packing density of the beaded dendritic regions, which usually were located in the periphery of the dendritic trees, were clearly lower than values obtained previously for cell bodies and proximal dendrites of a‐motoneurons.
Blood pressure response to angiotensin II in pregnant and lactating goats maintained on high or low sodium intake
Authors: OLSSON K. , DAHLBORN K. , KARLBERG B. E.
Published: December 2008

Goats were kept on either high (274 mmol day‐1) or low (68 mmol day‐1) sodium intake during pregnancy, lactation, and anoestrus. High salt (HS) animals had about three times greater renal Na excretion than low salt (LS) animals, but the differences in plasma volume, protein concentration, and haematocrit were generally not significant. Angiotensin II (All) was infused intravenously for 28‐min periods in doses of 0.30, 0.75, or 1.00 nmol min‐1. The increase in mean arterial blood pressure (MAP) during All infusions was greater in HS than in LS goats, but became attenuated in all animals during the course of the pregnancy. In LS goats the MAP rise was smaller in late pregnancy than during lactation and anoestrus. In HS goats the rise in MAP was exaggerated in early pregnancy and was similar to lactation and anoestrus values in late pregnancy. During lactation and anoestrus the goats showed similar MAP increase in response to All infusions. The pulse pressure was greater during All infusions performed in early pregnancy, lactation and anoestrus than in late pregnancy. Cardiac arrhythmias were noted during All infusions, most frequently during lactation and in HS goats in early pregnancy. The results show that a moderately elevated sodium intake causes a significantly higher MAP increase in response to All infusions during pregnancy. This abolishes the reduction of the MAP increase to All infusions during late pregnancy as compared to anoestrus; a phenomenon which is observed in goats on a low sodium intake.
Changes in cyclic 3'5‘‐adenosine monophosphate tissue concentration and net fluid transport in the cat's small intestine elicited by cholera toxin, arachidonic acid, vasoactive intestinal polypeptide and 5‐hydroxytryptamine
Authors: EKLUND S. , BRUNSSON I. , JODAL M. , LUNDGREN O.
Published: December 2008

We have analysed tissue cyclic 3'5′‐adenosine monophosphate (cAMP) concentration in different fractions of the cat's small intestinal mucosa during secretion elicited in vivo by four different secretagogues: cholera toxin (administered intraluminally), vasoactive intestinal polypeptide (VIP; given i.a.), arachidonic acid (AA; administered intraluminally) and 5‐hydroxytryptamine (5‐HT; given i.a.). Cholera toxin was found to increase cAMP concentration in the villi but not in the crypts. The VIP, AA and 5‐HT did not influence tissue cAMP concentration despite a profuse net fluid secretion. Hexamethonium inhibited secretion elicited by cholera toxin and AA but did not significantly influence tissue cAMP concentration. There is strong evidence for the view that villus and crypt regions of the small intestinal mucosa have different functions, secretion taking place in the crypts and absorption in the villi. However, the lack of cAMP increase in the crypts reported in this study suggests that cholera toxin in this model does not reach the crypts. The results are not in agreement with a role for cAMP in mediating secretion from the crypts, but are compatible with a role of cAMP in inhibiting absorption in the villi. It is suggested that the observed fluid secretion from the crypts elicited by cholera toxin, AA and 5‐HT is to a major part mediated by intramural enteric reflexes.
Functional role of aerobic glycolysis in rat portal vein
Authors: LÖVGREN B. , HELLSTRAND P.
Published: December 2008

The functional role of aerobic lactate production in the rat portal vein was investigated. Changing substrate from glucose (11.5 mM) to pyruvate (11.5 mM) or β‐hydroxybutyrate (3 mM) had virtually no effect on spontaneous mechanical activity. Lactate production (JLA) was smaller with pyruvate than with glucose (0.05 ± 0.01 vs. 0.14 ± 0.03 μmol g‐1 min‐1, n= 4).Addition of 0.5 mM iodoacetate to inhibit glycolysis abolished mechanical activity in 15–20 min with glucose as substrate, whereas with pyruvate the mechanical activity was only moderately reduced over this time period. With β‐hydroxybutyrate (3 mM) as substrate no aerobic lactate production was detected during normal spontaneous activity. Inhibition of cellular respiration with increasing concentrations of cyanide in β‐hydroxybutyrate medium led to a graded decrease in mechanical activity and JO2, but only a marginal increase in lactate production. With glucose as substrate, repeated stimulation with a combination of isoproterenol (10–5 M) and papaverine (10–4 M) gave similar increases in lactate production at each exposure. With β‐hydroxybutyrate some lactate production was found at the first stimulation, but decreased to be abolished at the third stimulation. The mechanical inhibition caused by the stimulation was however similar at the three exposures for both substrates. Lactate production induced by cAMP‐raising stimulation in β‐hydroxybutyrate could be accounted for by glycogenolysis. These results show that aerobic glycolysis leading to net lactate production is not necessary for normal spontaneous mechanical activity or the relaxing effect of hypoxia or cAMP raising stimuli in rat portal vein.
CNS‐induced natriuresis is not mediated by the atrial natriuretic factor
Authors: HANSELL P. , GÖRANSSON A. , LEPPÄLUOTO J. , ARJAMAA O. , VAKKURI O. , ULFENDAHL H.R.
Published: December 2008

Studies were performed on anaesthetized Wistar‐Kyoto rats to investigate whether the natriuretic response to stimulation of the cerebroventricular system with a hypertonic sodium solution is in part caused by increased plasma concentrations of atrial natriuretic factor (ANF).Through a cannula inserted into a lateral cerebral ventricle a solution with a normal (CSF, 152 mmoll‐1) or high (NaCSF, 1000 mmoll‐1) sodium ion content was infused. In the stimulated animals which received NaCSF, the sodium excretion increased more than 13‐fold, from 0.07 ± 0.02 (mean ± SEM) to 0.97 ± 0.22 μmol min‐1 g‐1 kidney wt (P < 0.01).Potassium excretion rose more than eight‐fold, from 0.37 ± 0.05 103.01 ± 0.13 μmol min‐1 g‐1 kidney wt (P < 0.001), and the urine flow rate more than seven‐fold, from 1.35±0.11 to 9.74±1.23μ min‐1 g‐1 kidney wt (P < 0.001).The mean arterial blood pressure increased from 100 ± 3 to 129±17 mmHg (P < 0.001).In the control animals which received CSF throughout the experiment there was no significant change in the above variables. The concentrations of ANF in plasma taken at the end of the experiments were determined by a radioimmunoassay. The mean plasma concentration of ANF in animals receiving CSF throughout the experiment was 175 ± 36 pg ml‐1.This was not significantly different from the corresponding value in animals which were given NaCSF (118 ± 34 pg ml‐1).In conclusion, stimulation of the cerebroventricular system with a hypertonic sodium solution induced marked increases in electrolyte excretion. The results of this study indicate that this effect is mediated by some other factor than ANF.
Arterial PCO2 and lung ventilation in man exposed to 1–5% CO2 in the inspired gas
Authors: ELLINGSEN I. , LIESTØL K. , SYDNES G. , HAUGE A. , NICOLAYSEN G.
Published: December 2008

Conflicting results have been published on the shape of the curve relating the change in lung ventilation to the change in alveolar or arterial PCO2 induced by increased inspired CO2 (the CO2 sensitivity). In this study eight human subjects with in‐dwelling arterial cannulae were each exposed to five different levels of increased inspired CO2 (1–5%). Arterial PCO2 and ventilation were measured in the 7th minute of each period of CO2 exposure. Each CO2 exposure period was flanked by control periods in which similar measurements were carried out during air breathing. We found non‐linear increases in both ventilation and arterial PCO2 with increasing levels of inspired CO2. When 5 % CO2 in air was inspired the arterial PCO2 increased by about 15% of the inspired CO2 load. There was no significant non‐linearity in the relation between change in alveolar ventilation (normalized to body surface) and change in arterial PCO2. The inter‐individual variation in CO2 sensitivity was less when alveolar ventilation was normalized to the CO2 output rather than to body surface area. We conclude that the sensitivity to CO2 is close to constant within the range 0–5 % CO2 in the inspired gas.
Permeability of renal capillaries. II. Transport of neutral and charged protein molecular probes
Authors: ÖJTEG G. , NYGREN K. , WOLGAST M.
Published: December 2008

The permselectivity of the renal capillaries was investigated from the transport of a series of molecular probes: (1) inulin, (2) positive (+ 2, net charge at pH 7.4), neutral (o), and negative (‐6) myoglobin, (3) neutral (0) and negative (‐14) horseradish peroxidase (HRP) and (4) two isomers of lactate dehydrogenase (LDH), namely the positively charged (+ 2) LDH‐M4 and the negatively charged (‐19) LDH‐H4. The determination of the concentration of tracer proteins necessitated gel separation of both plasma and renal hilar lymph. The reason for this is that the proteins, after filtration, will be reabsorbed and degraded by the proximal tubular cells into small molecular compounds (amino acids), which will return to both the renal interstitium and systemic plasma. Even if this degradation is of low degree, as for high‐molecular‐weight proteins, separation is still required, since the relative lymph concentration (plasma concentration put at 1) is also low, that is, even small amounts of low molecular compounds will distort the relative lymph concentration obtained. The transport from plasma to renal hilar lymph of the tracer molecules fell with increasing Stokes‐Einstein radius. The relative lymph concentration of the 11 Å inulin was 1.06 ± 0.03 (mean ± SEM), of the neutral 17.5 Å myoglobin 0.76 ± 0.05, of the neutral 32 Å HRP 0.32 ± 0.02 and of the neutral 46 Å LDH 0.12 ± 0.01. The data are compatible with a two‐pore system. The negative tracer molecules were in general proportionally more restricted than the neutral (or positive) moieties (P < 0.001) thus suggesting a negatively charged peritubular capillary membrane. The mass transport of the negative myoglobin and HRP was lower than that of the corresponding neutral moieties (P < 0.001), which indicates a negatively charged glomerular capillary membrane.
Autoradiographic location of β‐adrenoceptor subtypes in cat colon smooth muscle
Authors: EK B. , JODAL M. , LUNDGREN O.
Published: December 2008

In order to localize β‐adrenoceptors125I‐(—)pindolol (IPIN) was used in binding to sections from cat colon. The binding characteristics for IPIN to β‐adrenoceptors on colon sections were estimated by demonstrating reversible binding in the presence of isoprenaline and by steroselective binding to the isomers of propranolol. The binding of IPIN to both β1‐and β2‐adrenoceptors was shown by biphasic displacement curves in the presence of the selective β‐adrenoceptor compounds betaxolol, ICI 118.551 and procaterol. The colon sections were found to contain proportions of β1‐adrenoceptors (30–50%) and β2‐adrenoceptors (50–70%). In the autoradiographic studies, 100% of the developed grains after exposure of IPIN to the photographic emulsion were displaced by 50 μmof isoprenaline. By microscopic counting at autoradiographic grains, 30–40% of the grains were found in the circular smooth muscle, while 60–70% of the grains were found in the longitudinal smooth muscle. A concentration of 2 nmICI 118.551 completely displaced all grains in the circular smooth muscle and partly displaced those found in the longitudinal smooth muscle. A high concentration of ICI 118.551 (1 μm) displaced all grains above background from the smooth muscle. It is concluded that the circular smooth muscle only contains β2‐adrenoceptors, while longitudinal smooth muscle may contain a proportion of β1‐adrenoceptors. Whether such a location of β‐adrenoceptors can be related to the β1‐adrenoceptor‐mediated inhibition of colon motility can not be clarified from these studies. However, it seems that β1‐adrenoceptors are located to the longitudinal smooth muscle instead of to the myenteric plexus of the colon.
The influence of Atriopeptins I and II on the relationship between glomerular filtration and natriuresis
Authors: HANSELL P. , ULFENDAHL H. R.
Published: December 2008

The effects of two pure synthetic atrial natriuretic factors, Atriopeptin (AP) I and AP II, on the whole kidney glomerular filtration rate (GFR), sodium and potassium excretion (UNa V, UK V), urine flow rate (V) and arterial blood pressure (BP) were studied in adult male Sprague‐Dawley rats. The variables were measured during a control period and during 70 min of continuous intravenous infusion of AP I or AP II at a rate of 10 μg h‐1 kg‐1 body wt. A time control group was studied in parallel to see whether the variables under study changed with time. The AP I infusion did not affect GFR (change from 1.34 ± 0.10 to 1.24 ± 0.04 ml min‐1 g‐1 kidney wt), but was clearly natriuretic (UNa V changed from 0.071 ± 0.011 to 0.229 ± 0.038 μmol min‐1 g‐1 kidney wt, P < 0.01). The UK V increased from 0.504 ± 0.073 to 1.138 ± 0.121 μmol min‐1 g‐1 kidney wt, (P < 0.001) and V from 1.88 ± 0.10 to 2.94 ± 0.15 μl min‐1 g‐1 kidney wt, (P < 0.001). Urine osmolality (Uosm) and BP were unaffected. During AP II infusion GFR remained unchanged but was slightly below the pre‐infusion level during the last infusion period (1.05 ± 0.07 as against 1.37 ± 0.09 ml min‐1 g‐1 kidney wt, P < 0.05). Despite this fact, UNa± was significantly elevated throughout the infusion period. The UNa V increased from 0.100 ± 0.008 in the control period to 1.404 ± 0.432 μmol min‐1 g‐1 kidney wt (P < 0.01) after 50 min of infusion. During the period when GFR was slightly below the pre‐infusion level, UNa V was 1.364 ± 0.434 μmol min‐1 g‐1 kidney wt (P < 0.001). The UK V increased from 0.610 ± 0.175 in the control period to 1.266 ± 0.142 μmol min‐1 g‐1 kidney wt (P < 0.05). The urine flow rate increased from 1.95 ± 0.17 to 5.47 ± 0.88 μl min‐1 g‐1 kidney wt (P < 0.01), and Uosm decreased from 1922 ± 90 to 1644 ± 99 mosm kg‐1 H2O (P < 0.05), whilst BP fell from 114 ± 2 to a steady‐state level of 98 ± 3 mmHg (P < 0.001). It is concluded that Atriopeptin I and Atriopeptin II increase sodium excretion mainly by affecting tubular transport processes. Through its vascular effects, Atriopeptin II will also decrease the arterial blood pressure and, as previously shown, transiently increase medullary blood flow, and the latter increase may contribute to the natriuretic response.
Muscle sympathetic activity and venous plasma noradrenaline concentrations during static exercise in normotensive and hypertensive subjects
Authors: WALLIN B.G. , MÖRLIN C. , HJEMDAHL P.
Published: December 2008

Peroneal muscle sympathetic activity (MSA) was recorded during 2 min of isometric handgrip at 30% of maximal power and correlated with plasma levels of noradrenaline (NA) in venous blood from the contralateral forearm in 16 normotensive subjects and 15 previously untreated patients with essential hypertension. Resting values for MSA and NA were similar in the two groups and there was a significant positive correlation between the level of MSA (expressed either as bursts per 100 heart beats or bursts min‐1) and the concentration of NA.Changes of MSA and NA during handgrip were similar in both groups. When monitored every minute in a subgroup of the material (n= 12), the number of sympathetic bursts min‐1 increased maximally by 23% and total MSA (bursts min‐1 mean burst amplitude) by 67% during the second minute of handgrip. The maximal increase of venous NA concentrations was 21% and occurred 2 min later, probably reflecting a slow wash‐out of NA from the neuroeffector junctions. It is concluded that: (1) there is no difference in MSA between normotensive and hypertensive subjects at rest or during isometric handgrip, (2) MSA is an important determinant of the concentration of NA in forearm venous plasma, and (3) the relative change of the venous plasma NA concentration during isometric handgrip is considerably smaller than the change in total MSA.
Terbutaline and budesonide as inhibitors of postischaemic permeability increase
Authors: PERSSON N.H. , ERLANSSON M. , BERGQVIST D. , TAKOLANDER R. , SVENSJÖ E.
Published: December 2008

A temporary ischaemia with total circulatory arrest of the hamster cheek pouch was obtained by clamping the neck of the everted cheek pouch. The macromolecular permeability increase in postcapillary venules was quantified as the leakage of fluoroscein‐labelled dextran using intravital microscopy and a fluorometer simultaneously. At reperfusion after 30 min ischaemia, there was a significant and reversible permeability increase. This response could be totally prevented by topical administration of either terbutaline, a selective β2‐receptor agonist, or budesonide, a glucocorticoid, but it was not significantly impeded by the antihistamine mepyramine. The study shows that, in conformity with the situation in inflammation, the postischaemic permeability increase at reperfusion after ischaemia can be blocked by either β2‐stimulation or glucocorticoids. Furthermore, it indicates that histamine, a common inflammatory mediator, is not responsible for the postischaemic permeability increase.
[3H]noradrenaline efflux from platelets and synaptosomes of ethanol‐treated rats
Authors: ÖHLIN H. , MATTIASSON I. , CHRISTENSSON B. , NYSTRÖM I. , HOOD B.
Published: December 2008

Platelets have the ability to take up, store and release biogenic amines and have therefore been used as models for neurons in studies of neuropsychiatric disorders and hypertension. We have studied the spontaneous efflux of [3H]noradrenaline from platelets and synaptosomes of rats chronically treated with ethanol. Male control rats had a more rapid [3H]noradrenaline efflux both from synaptosomes and platelets than female control rats. Ethanol treatment increased efflux in female rats, again both in platelets and synaptosomes. These results suggest that a parallelism exists in noradrenline release between synaptosomes and platelets, both basal and in situations which stimulate the release.
Conditions for increased cardiac output during occlusion of the descending thoracic aorta
Authors: VENGEN Ø.A. , ILEBEKK A.
Published: December 2008

Previous studies have demonstrated that occlusion of the descending thoracic aorta (AO) at constant heart rate induces a rise in stroke volume during a continuous intravenous (i. v.) isoproterenol infusion, but no change in stroke volume during a selective inotropic stimulation of the left ventricle as achieved by an intracoronary (i. c.) isoproterenol infusion. To determine the mechanism for this difference in stroke volume response, the haemodynamic adjustments of both the right and the left ventricle to AO during continuous i. v.and i. c.isoproterenol infusion in anesthetized open‐chest pigs were compared. The AO induced a similar rise in left ventricular systolic pressure and end‐systolic segment length (measured by an ultrasonic technique) in both ventricles whether isoproterenol was infused i. v.or i. c., but stroke volume rose by 26.3 (11.9–38.1%) (median and 95% confidence interval) (P < 0.01) during i. v., compared with 3.8 (‐7.4–14.7)% (n. s.) during i. c.isoproterenol infusion (difference in response: P < 0.01). End‐diastolic segment length increased more by AO during i. v.than i. c.isoproterenol infusion; 7.8 (5.1–16.9)%vs. 5.7 (3.1–8.5)% (difference in response: P < 0.01) in the left ventricle, and 5.9 (3.5–8.1)%vs. 1.0 (‐1.5–3.3)% (difference in response: P < 0.01) in the right ventricle. Redistribution of blood through the inferior caval vein measured immediately after AO, amounted to 130 (110–172) ml during i. v.and to 77 (52–89) ml during i. c.isoproterenol infusion (n= 3). Thus, greater blood volumes were redistributed, causing the end‐diastolic segment length in both ventricles to be more increased during AO when isoproterenol was administered i. v.than selectivity (i. c.) to the left ventricular myocardium.
Methionine‐induced acidosis in the weanling rat
Authors: WAMBERG S. , ENGEL K. , KILDEBERG P.
Published: December 2008

Whole body balances of non‐metabolizable base (NB) were studied in weanling rats fed a cereal‐based diet with or without added l‐methionine. In response to l‐methionine loading (2.5 mmol day‐1) the rats exhibited a significant reduction in rates of food intake (109 vs. 160 g per 8 days) and body growth (3 vs. 52 g per 8 days); fractional oxidation of absorbed dietary amino acid sulphur increased from 0.28 to 0.64; and mean urinary sulphate excretion increased from 2.3 to 14.8 mmol per 8 days. Mean rates of renal excretion of NB and filtered titratable organic acid decreased from 20 to −11 mmol per 8 days and from 22 to 8 mmol per 8 days. Balances of calcium and NB remained at reference values despite a decrease in whole blood ‘base excess’ from −1.0 to −6.4 mmol 1–1. The concentration of NB in plasma rose but slightly. It is concluded that L‐methionine loading in the weanling rat leads to extracellular non‐carbonic acidosis subject to renal compensation. This acidosis is due not to retention of H+ released by ionization of endogenous sulphuric acid but possibly to accumulation of (acid) organic metabolites of methionine which are efficiently conserved by the kidneys. The rise in sulphuric acid production leads to an adaptive decrease in fractional reabsorption of filtered sulphate. Even during inhibited growth, absorbed dietary NB is retained and deposited in the skeleton, probably as calcium carbonate.
Reflex changes in sympathetic nerve activity during mechanical ventilation with PEEP in sino‐aortic denervated rats
Authors: SELLDÉN H. , DELLE M. , SJÖVALL H. , RICKSTEN S.‐E.
Published: December 2008

The aim of this study was to evaluate the role of cardiopulmonary receptors with vagal afferents in the reflex control of sympathetic nerve activity during mechanical ventilation with positive end‐expiratory pressure (PEEP). Experiments were performed on 17 chloralose‐anaesthetized rats. Changes in renal sympathetic nerve activity (RSNA), heart rate and mean arterial pressure were studied at zero end‐expiratory pressure (ZEEP) and at 5 and 10 cm H2O PEEP in intact animals (n = 8), after sino‐aortic denervation (n = 17) and after sino‐aortic denervation plus vagotomy (n = 10). In the intact animals, 10 cm H2O PEEP induced a significant increase in RSNA (+ 66%) and heart rate(+10%)while the mean arterial pressure did not change significantly. Sino‐aortic denervation increased baseline levels of RSNA, heart rate and mean arterial pressure. After sino‐aortic denervation, 10 cm H2O PEEP still induced a significant increase in RSNA (+ 22 %) and heart rate in 13 animals. In four animals, 10 cm H2O PEEP elicited a depressor reflex with a significant decrease in both RSNA (— 32%) and heart rate. Bilateral vagotomy after sino‐aortic denervation at ZEEP significantly increased RNSA (+15%) and heart rate, indicating an ongoing tonic inhibitory influence on RSNA from vagal afferents in sino‐aortic denervated rats. The PEEP did not induce any significant change in RSNA or heart rate after sino‐aortic denervation plus vagotomy. The results indicate that cardiopulmonary receptors with vagal afferents contribute to the reflex excitation of the sympathetic nervous system during mechanical ventilation with PEEP. Under certain circumstances, PEEP may also trigger powerful depressor reflexes, mediated by vagal afferents.
Vasodilatory effects and coexistence of calcitonin gene‐related peptide (CGRP) and substance P in sensory nerves of cat dental pulp
Authors: GAZELIUS B. , EDWALL B. , OLGART L. , LUNDBERG J. M. , HÖKFELT T. , FISCHER J. A.
Published: December 2008

Substance P (SP)‐ and calcitonin gene‐related peptide (CGRP)‐immunoreactivity (‐IR) were localized by immunohistochemistry in the same nerve cell bodies in the trigeminal ganglia as well as in nerve terminals of the dental pulp. The distributions of SP‐ and CGRP‐IR nerves were identical in the dental pulp and mainly associated with blood vessels. The level of CGRP‐IR in the dental pulp, as measured by radio‐immunoassay (RIA), was 1.4±0.2 pmol g‐1 wet wt, which is in the same range as that found for substance P. Local intra‐arterial infusion of synthetic CGRP and substance P produced vasodilatation in the dental pulp as measured by both laser Doppler flowmetry and an 1251 clearance technique. The CGRP was effective as a vasodilator when infused in the femtomole per minute range, and SP in the picomole range. The effect of CGRP (50 fmol min‐1) was 10 times larger when given after SP (15 pmol min‐1) than before it. Since the two peptides coexist in the same neurons, it is suggested that they both contribute to the vasodilatation seen upon antidromic stimulation of sensory nerves.
L‐vasopressin inhibits oxytocin‐induced increases of plasma levels of insulin in conscious dogs
Authors: STOCK S. , UVNÄS‐MOBERG K.
Published: December 2008

Oxytocin is known to increase plasma levels of insulin, glucagon and glucose in dogs. Plasma levels of vasopressin rise during stressful conditions. Since vasopressin counteracts several oxytocin‐induced effects, it was decided to study how vasopressin influences the oxytocin‐induced elevation of plasma levels of insulin, glucagon and glucose. Therefore oxytocin at 0.11 (which gives rise to physiological plasma concentrations) was infused i.v. for 10 min into fasted, conscious dogs either alone or in combination with 0.033 or 0.17 nmol kg‐1 h‐1 of L‐vasopressin. Accordingly, 1.1 nmol kg‐1 h‐1 of oxytocin was infused alone or in combination with 0.67 or 1.7 nmol kg‐1 h‐1 of L‐vasopressin. Repeated blood samples were drawn during and after the infusions and insulin and glucagon levels were determined by radio‐immunoassay. Plasma levels of insulin increased three‐ and six‐fold in response to 0.11 and 1.1 nmol kg‐1 h‐1 of oxytocin, respectively, and the elevations were inhibited by L‐vasopressin. Slight (1.5–fold) increases in plasma levels of glucagon were observed following 0.11 and 1.1 nmol kg‐1 h‐1 of oxytocin, although the effect was significant only after the latter dose. Concomitant infusion with L‐vasopressin did not markedly influence the effect caused by oxytocin. Small, insignificant increases in blood glucose levels were induced by both doses of oxytocin. These effects were not affected by concomitant infusions of L‐vasopressin. The insulin levels rose before glucose levels suggesting that oxytocin stimulates the release of insulin without a previous rise in glucose levels. In conclusion, it has been shown that vasopressin, in amounts which give rise to physiological plasma concentrations, inhibits oxytocin‐induced effects on insulin levels, and that oxytocin stimulates the release of insulin via a mechanism which is independent of elevations in blood glucose levels.
Leakiness of rat brain microvessels to fluorescent probes following craniotomy
Authors: OLESEN S. P.
Published: December 2008

The effects of craniotomy and/or histamine treatment upon brain microvascular permeability was studied in Wistar rats. Extravasation of circulating Na‐fluorescein (MW 376) and of FITCalbumin (MW 69,000) was observed through a cranial window using intravital fluorescence microscopy. Simple exposure of the pial microvessels induced formation of discrete spots of fluorescent material around venules, but not around arterioles or capillaries. The average number of leaky spots to Na‐fluorescein and to FITC‐albumin was 4.3 and 1.8 per 10mm2, respectively, 35 min after exposure. Pretreatment of the rats with either indomethacin (a cyclo‐oxygenase inhibitor) or promethazine (a histamine H1‐receptor blocker) did not reduce the number of leaky sites, whereas pretreatment with a combination of the two drugs had a significant protective effect. Administration of histamine (10–4 M) to the exposed brain surface for 5 min increased the number of leaky sites to Na‐fluorescein and FITCalbumin 3.2 and 3.6 times, respectively. It is concluded that exposure of the brain surface induces release of histamine and cyclo‐oxygenase metabolites, and that these inflammatory mediators elicit formation of leaky sites in brain venules.
Effects of N‐ethylmaleimide and forskolin on noradrenaline release from rat hippocampal slices. Evidence that prejunctional adenosine and a‐receptors are linked to A/‐proteins but not to adenylate cyclase
Authors: FREDHOLM B. B. , LINDGREN E.
Published: December 2008

N‐ethylmaleimide (NEM) treatment has been shown to inactivate regulatory GTP‐binding N (G)‐proteins in many preparations, including slices of rat hippocampus. NEM‐treatment (100 μM for 15 min) has been used to examine the possible involvement of a N‐protein in the prejunctional inhibitory effect of an adenosine analogue, R‐PIA acting on A,‐receptors, and of clonidine acting on a,‐adrenoceptors in this tissue. NEM treatment significantly enhanced basal overflow of [3H]NA and the overflow stimulated by low (0.3 Hz) frequency stimulation, but not the overflow stimulated by higher (1–10 Hz) frequency stimulation. The prejunctional inhibitory effect of R‐PIA (I μM) on NA release, stimulated by a 3 Hz stimulation, was abolished by NEM pretreatment, which also eliminated the dosedependent prejunctional effect of clonidine and reduced the facilitatory effect of yohimbine. Forskolin had a small, but significant stimulatory effect on NA overflow, but did not reduce the prejunctional inhibitory effect of R‐PIA. The adenylate cyclase inhibitor SQ22, 536did not reduce NA overflow. These results show that NEM blocks a critical step in the prejunctional action of both adenosine‐and a,‐receptor agonists, which may be a N‐protein. The possibility is discussed that the prejunctional A,‐ and a,‐receptors couple to aN‐protein that controls a different effector than adenylate cyclase.
Characterization of an in vitro perfused rat ovary model: ovulation rate, oocyte maturation, steroidogenesis and influence of PMSG priming
Authors: BRÄNNSTRÖM M. , JOHANSSON B. M. , SOGN J. , JANSON P. O.
Published: December 2008

An in nitro perfused rat ovary model was characterized with respect to ovulation rate, oocyte maturation and steroidogenesis after priming with various doses of pregnant mare's serum gonadotrophin (PMSG) (10, 20 or 30 IU PMSG S.C. in the morning of day 28). In ovaries stimulated with LH 0.1 μg m1‐‐1 after 1 h of perfusion the number of ovulations was significantly higher in the 20 IU PMSG group than in the 10 IU PMSG group (6.8±1.0 ovulations per treated ovary versus 2.4±1.2, P < 0.01). Priming with 30 IU PMSG did not result in significantly more or fewer ovulations than did 10 or 20 IU PMSG. No ovaries in the non‐stimulated control groups ovulated. Oocytes retrieved directly at ovulation were mature (GVB or PB stage). Among oocytes retrieved from pre‐ovulatory follicles punctured at 0, 2, 4, 6 and 8 h after stimulation with LH 0.1 μg ml‐1 thtre was an increasing number of oocytes with GVB (0/10 at oh and 10/10 at 8 h). Stimulation with LH resulted in a rapid release of progesterone, testosterone and oestradiol into the medium, whereas non‐stimulated control ovaries exhibited a slow rise of all steroids throughout the perfusion period. It is concluded that priming with 20 IU PMSG in this model results in an optimal number of ovulations and that this model provides a useful tool in studies of various kinds of modifying influences on the ovulatory process.
Effects of chronic stimulation on the size and speed of long‐term denervated and innervated rat fast and slow skeletal muscles
Authors: HENNIG R. , LØMO T.
Published: December 2008

This study seeks to identify the mechanisms which motoneurones use to control the contractile force and speed of skeletal muscles. We have stimulated directly slow soleus (SOL) and fast extensor digitorum longus (EDL) muscles of adult rats intermittently at 100 Hz for 1–9 months. The muscles were either chronically denervated, denervated and reinnervated, or normally innervated. The stimulation started either immediately, or more commonly, after 1–9 months of denervation. Stimulation starting several months after denervation increased the mean maximum tetanic tension 37 times in SOL and eight times in EDL. These values represented 40 and 12% of the increases obtained by reinnervation after comparable periods of time. In denervated SOL and EDL muscles stimulated directly for more than 2 months, the mean isometric twitch contraction times were 13 and 12.7 ms, as in normal EDL muscles (13 ms). In innervated SOL muscles stimulated directly for 1–4 months, the mean twitch contraction times were 23.6 ms (normally innervated) and 19.2 ms (reinnervated), which were considerably shorter than in normal control SOL muscles (39.2 ms). Single motor unit recordings revealed that the natural (background) nerve impulse activity was essentially unaffected by the stimulation. Twitch contraction time and percentage of type II fibres in SOL muscles were related. The fastest muscles (denervated and stimulated) consisted of 100% type II fibres (with one exception), the second fastest (reinnervated and stimulated) of 70–50%, the third fastest (normally innervated and stimulated) of 45–0%, the second slowest (reinnervated) of 15–0%, and the slowest muscles (innervated controls) of 5–0% type II fibres.
Anabolic steroids alter the haemodynamic responses of the canine left ventricle
Authors: RÄMÖ P.
Published: December 2008

The effect of an anabolic steroid on canine left ventricular function was studied by catheterization exposing control (n= 7) and methandienone‐treated (n = 6) dogs to pacing, volume and isoproterenol tests at the beginning of the experiment and 6 weeks later. The physical performance of the animals was evaluated by submaximal exercise test (SMT), in which the steroid‐treated dogs had lower heart rate than the sedentary controls (P < 0.001). Heart weight was greater in the steroid than in the control group (P < 0.05). Isoproterenol infusion increased the maximum value of the left ventricular pressure curve (dP/dtmax) less in the steroid‐treated than in the control animals (P < 0.05). Also heart rate was lower in the steroid than in the control group after inotropic load, while end‐diastolic, end‐systolic and stroke volumes decreased significantly more in the control group (P < 0.05). Systemic vascular resistance decreased in the steroid treated animals, but remained unchanged in the control group (P < 0.05 between the groups). During volume overload dP/dtmax increased in the control group but decreased slightly in the steroid group (P < 0.05 between the groups). The pressurevolume diagram showed that the left ventricle of the steroid‐treated animals worked on higher ventricular volumes than in the control group. In conclusion, long‐term methandienone treatment results in cardiac hypertrophy in dogs, reduces its response to an inotropic load and leads to working on larger ventricular volumes.
Antrum participates in the postprandial augmentation of the acid response to exogenous gastrin in conscious cats
Authors: FERNSTRÖM M. , UVNÄS‐MOBERG K. , EMÅS S.
Published: December 2008

A humoral mechanism, potentiating the maximal acid, but not th: pepsin response to exogenous gastrin in cats, is activated by protein‐rich food in the stomach or duodenum, but not in the jejunum. In the present study, the effect of an oral meat meal on the maximal acid response to pentagastrin was investigated in Heidenhain pouch (HP) cats, and in antrectomized HP cats with duodenal exclusion and gastrojejunostomy Roux‐en‐Y. Antrectomy and duodenal exclusion abolished the postprandial HP acid response, and feeding did not potentiate the acid response to pentagastrin. The finding suggests that the gastrin‐potentiating mechanism in the stomach is localized in the antrum, and it cannot be demonstrated in the jejunum. The basal plasma levels of gastrin and somatostatin did not differ in antrectomized and non‐antrectomized cats. Antrectomy and duodenal exclusion abolished the postprandial gastrin and somatostatin responses. The plasma somatostatin increase during pentagastrin infusion persisted after antrectomy and duodenal exclusion. It is concluded that the antrum is not mandatory for the basal plasma levels of gastrin and somatostatin, but the postprandial gastrin response is of antral origin and may release somatostatin. Pentagastrin infusion releases extra‐antral somatostatin in cats.