bluuebunny/crossref_metadata_2025 huggingface dataset:
Subcutaneous and skeletal muscle vascular responses in human limbs to lower body negative pressure
Authors: JACOBSEN T.N. , NIELSEN H.V. , KASSIS E. , AMTORP Ø.
Published: December 2008

Jacobsen, T. N., Nielsen, H. V., Kassis, E. & Amtorp oS. 1992. Subcutaneous and skeletal muscle vascular responses in human limbs to lower body negative pressure.Acta Physiol Scand144, 247–252. Received 8 March 1991, accepted 7 Novcmber 1991. ISSN 0001–6772. Department of Cardiology, Gentofte Hospital, University of Copenhagen, Denmark

Cardiopulmonary baroreceptor unloading in humans comparably increases sympathetic discharge to skeletal muscle in the forearm and calf, but blood flow studies have disclosed differential rather than uniform vasomotor responses in the extremities. The aim of the present study was to address the issue of differential effects of orthostatic stress on forearm and calf vascular adjustment and to extend previous studies by determining changes in vascular responses separately in various vascular beds of the limbs. The local [133Xenon] washout method was used for recording blood flow rates in subcutaneous tissue and skeletal muscle. Simultaneous recordings from the forearm and calf were performed in 11 healthy young males during lower body negative pressure at —10 mmHg. Heart rate, arterial mean and pulse pressures did not change during lower body negative pressure. In the forearm blood flow rates decreased significantly, in subcutaneous tissue by 16 ± 2% (mean ± SEM) and in skeletal muscle by 16 ± l%. In the calf lower body negative pressure induced a significant decrease in blood flow rates of 17 ± 3% in subcutaneous tissue and of 30 ± 2% in skeletal muscle. This vasoconstriction in calf skeletal muscle was consistently disclosed in both legs and was about the same magnitude in each calf when studied with the one leg exposed to lower body negative pressure and the other outside the lower body negative pressure chamber. These findings suggest that during unloading of cardiopulmonary afferents, reflex sympathetic activation as an important autonomic adjustment to orthostatic stress is accompanied by uniform vasoconstriction in subcutaneous and skeletal muscle vascular beds of human limbs.
High salt diet down‐regulates proximal tubule Na+, K+‐ATPase activity in Dahl salt‐resistant but not in Dahl salt‐sensitive rats: evidence of defective dopamine regulation
Authors: NISHI A. , BERTORELLO A. M. , APERIA A.
Published: December 2008

Nishi, A., Bertorello, A. M. & Aperia, A. 1992. High salt diet down‐regulates proximal tubule Na+, K+‐ATPase activity in Dahl salt‐resistant but not in Dahl salt‐sensitive rats; evidence of defective dopamine regulation. Acta Ptiysiol Scand144, 263–267. Received 26 July 1991, accepted 25 October 1991. ISSN 0001–6772. Department of Paediatrics, Karolinska Institute, Sweden

We examined the regulation of Na+, K+‐ATPase activity in proximal tubule segments during a high salt diet in prehypertensive Dahl salt‐sensitive and salt‐resistant rats. Rats were placed on normal salt or high salt diets (0.9% saline as drinking water). During the normal salt diet, Na+, K+‐ATPase activity was not different between Dahl salt‐sensitive and salt‐resistant rats. After 2 days and 10 days on a high salt diet, Na+, K+‐ATPase activity in Dahl salt‐resistant rats significantly decreased when compared to Dahl salt‐resistant rats on a normal salt diet (P < 0.01). The decreased Na+, K+‐ATPase activity in Dahl salt‐resistant rats during a high salt diet was reversed by treatment with an inhibitor of aromatic l‐amino acid decarboxylase (dopamine synthesizing enzyme), benserazide. In contrast, Na+, K+‐ATPase activity did not decrease during the high salt diet and benserazide had no effect on Na+, K+‐ATPase activity in Dahl salt‐sensitive rats. These results indicate that Dahl salt‐sensitive rats do not have the capacity to down‐regulate the proximal tubule Na+, K+‐ATPase activity during a high salt diet. Indirect evidence suggests that the regulation of Na+, K+‐ATPase activity by locally produced dopamine is absent in Dahl salt‐sensitive rats.
Trophic effects of hypophyseal hormones on resistance vessels and the heart in normotensive and renal hypertensive rats
Authors: FOLKOW B. , ISAKSSON O. G. P. , KARLSTRÖM G. , LEVER A. F. , NORDLANDER M.
Published: December 2008

Folkow, B., Isaksson, O. G. P., Karlström, G., Lever, A. F. & Nordlander, M. 1992. Trophic effects of hypophyseal hormones on resistance vessels and the heart in normotensive and renal hypertensive rats.Acta Physiol Scand144, 291–306. Received 20 June 1991, accepted 7 October 1991. ISSN 0001–6772. Department of Physiology, University of Goteborg, Sweden, and MRC Blood Pressure Unit, Western Infirmary, Glasgow, Scotland, UK.

Arterial pressure is an important determinant of cardiovascular structure and relates positively to it. The purpose of this study was to determine whether pituitary hormones influence the relation of pressure and structure. Male Sprague‐Dawley rats, aged 5 weeks, were studied in three groups: the first underwent hypophysectomy; the second was hypophysectomized but received replacement therapy with growth hormone and thyroxine; the third served as controls. Four days later half of each group underwent unilateral renal artery clipping, the other half serving as normotensive controls. For 5 weeks estimates were made of systolic blood pressure, heart rate, body weight and plasma renin activity. Rats were then killed; left ventricular, kidney and adrenal weights were determined and, using hindquarter perfusion, estimates were made of resistance at maximal dilatation (reflecting inner radius), and of maximal pressor response (reflecting wall thickness). Results: (1) Hypophysectomy in non‐clipped rats reduced growth rate, systolic blood pressure and heart rate while plasma renin activity rose. As related to pressure and to body weight, resistance at maximal dilatation, maximal pressor response, left ventricular weight remained at the juvenile values of a 5‐week‐old rat. Hormone replacement restored values to those of control rats aged 11 weeks. (2) Clipping in the control group rats increased systolic blood pressure more than in hypophysectomized and growth hormone and thyroxine receiving hypophysectomized groups even though plasma renin activity remained higher in hypophysectomized than in control rats. Plasma renin activity was highest in hypophysectomized rats with highest pressure. (3) Systolic blood pressure related positively to left ventricle weight, resistance at maximal dilatation, maximal pressor response and calculated wall thickness to inner radius ratios in all groups. However, these regressions were all, like renal structural adaptation, considerably depressed in the hypophysectomized group. Hormone replacement restored the relation of structure and pressure towards that of control group rats. Thus, growth hormone and thyroxine influence maturation of the normal cardiovascular system and greatly enhance its structural upward resetting in hypertension.
Plasma levels of oxytocin after food deprivation and hypoglycaemia, and effects of 1–deamino‐2–D‐Tyr—(OEt)‐4–Thr‐8–Orn‐oxytocin on blood glucose in rats
Authors: BJÖRKSTRAND E. , ERIKSSON M. , UVNÄS‐MOBERG K.
Published: December 2008

Björkstrand, E., Eriksson, M. & Uvnäs‐Moberg, K. 1992. Plasma levels of oxytocin after food deprivation and hypoglycaemia, and effects of l‐deamino‐2–D‐Tyr‐(OEt)‐l‐Thr‐8–Om‐oxytocin on blood glucose in rats. Acta Physiol Scand144, 355–359. Received 1 March 1991, accepted 25 October 1991. ISSN 0001–6772. Department of Pharmacology, Karolinska Institute, Sweden.

Oxytocin has been shown to influence insulin, glucagon and blood glucose levels in various experimental situations. The present study was performed in order to obtain support for a possible interaction of glucose and oxytocin under physiological conditions. We therefore studied whether or not short‐term food deprivation (24 hours) affects basal oxytocin levels in male, female and lactating rats, since this is a situation when glucose is mobilized to prevent hypoglycaemia. Secondly, we studied whether oxytocin levels rise in a situation when blood glucose levels fall, i.e. following i.p. injection of insulin (20 U kg‐1). In order to explore the role of oxytocin more directly, we investigated whether i.p. injection of the oxytocin antagonist 1–deamino‐2–D‐Tyr‐(OEt)‐4–Thr‐8–Orn‐oxytocin affects blood glucose levels. Plasma levels of oxytocin, insulin and glucagon were measured with radioimmunoassay in samples obtained after decapitation. We found that oxytocin levels were significantly increased following short‐term food deprivation in lactating rats. We also found that insulin‐induced hypoglycaemia could elevate plasma levels of oxytocin in female and male rats. In addition, administration of an oxytocin antagonist cause a small, hut significant decrease in blood glucose levels after 30 min. These data imply that oxytocin may he one of several factors that take part in the control of blood glucose regulation.
The modulatory effects of prostaglandins on both excitatory and inhibitory non‐adrenergic non‐choIinergic neurotransrnission in guinea‐pig airways
Authors: JOHANSSON‐RYDBERG I. G. M. , ANDERSSON R. G. G. , GRUNDSTRÖM N.
Published: December 2008

Johansson‐Rydberg, I. G. M., Andersson, R. G. G. & Grundström, N. 1992, The modulatory effects of prostaglandins on both excitatory and inhibitory non‐adrenergic non‐cholinergic neurotransmission in guinea‐pig airways. Acta Physiol Scand144, 439444. Received 28 August 1991, accepted 20 November 1991. ISSN 0001–6772. Department of Pharmacology, University Hospital of Linkoping, Sweden.

Guinea‐pig trachea and bronchi were used to investigate the effects of indomethacin and prostaglandin E2 (PGE2) on non‐adrenergic non‐cholinergic excitatory (e‐NANC) and inhibitory (i‐NANC) neurotransmission evoked by electrical field stimulation. Indomethacin potentiated e‐NANC responses in bronchi with intact epithelium but had no effect on epithelium‐denuded preparations. Inhibitory NANC responses were increased by indomethacin independent of the epithelium. Both i‐NANC and e‐NANC neurotransmission were suppressed by PGE2 in a dose‐dependent manner. These results indicate that endogenous prostaglandins (e.g. PGE2) generated from the epithelium have an inhibitory effect on i‐NANC and e‐NANC nerve responses in airways. The epithelium is presumably not the only source for generation of prostaglandins that are involved in i‐NANC neurotransmission.
The canine internal carotid system: regional differences in reactivity to nerve stimulation, noradrenaline and 5–hydroxytryptamine
Authors: NAVA‐HERNANDEZ E. , VALLE J. , GARCIA‐VILLALON A. L. , GARCIA J. L. , MONGE L. , GOMEZ B. , DIEGUEZ G.
Published: December 2008

Nava‐Hernandez, E., Valle, J., Garcia‐Villalon, A. L., Garcia, J. L., Monge, L., Gomez, G. & Dieguez, G. 1992. The canine internal carotid system: regional differences in reactivity to nerve stimulation, noradrenaline and 5–hydroxytryptamine. Acta Physiol Scand144, 4455452. Received 22 July 1991, accepted 5 November 1991. ISSN 0001–6772. Departamento de Fisiología, Universidad Autónoma de Madrid, Spain.

Reactivity of the canine internal carotid system to field electrical stimulation, noradrenaline and 5–hydroxytryptamine was determined isometrically using 4–mm cyclindrical rings from the cervical and cavernous portions and middle cerebral artery. Electrical stimulation at supramaximal voltage (0.54 Hz, 0.2 ms duration) produced a frequency‐dependent contraction that was similar in cervical and cavernous portions and lower in the middle cerebral artery. This response was blocked by tetrodotoxin (10‐6m)or phentolamine (10‐6m). Noradrenaline (10‐9‐3 × 10‐4m)produced concentration‐dependent contractions and the sensitivity was: cervical portion = cavernous portion > middle cerebral artery, and this effect was blocked by phentolamine (10‐6m). 5–hydroxytryptamine (10‐9‐‐10‐5m)caused concentration‐dependent contractions and the sensitivity was: cervical portion < cavernous portion < middle cerebral artery. This response was depressed by lysergic acid diethylamide (10‐6m). The results indicate that reactivity of the internal carotid system: (a) to alpha adrenergic activation by endogenous and exogenous noradrenaline is lower in the distal segment (middle cerebral artery) than in the proximal segments (cervical and cavernous internal carotid artery) and (b) to tryptaminergic activation increases as it courses toward the brain. Therefore, functional characteristics could be related to embryological origin which the segments of this vascular system are derived from.
Voltage‐sensitive calcium channels in a human small‐cell lung cancer cell line
Authors: PANCRAZIO J. J. , OIE H. K. , KIM Y. I.
Published: December 2008

Pancrazio, J.J., Oie, H.K. & Kim, Y.I. 1992. Voltage‐sensitive calcium channels in a human small‐cell lung cancer cell line.Acta Physiol Scand144, 463468. Received 1 October 1991, accepted 24 October 1991. ISSN 0001–6772. Departments of Biomedical Engineering and Neurology, University of Virginia Health Sciences Center, and the National Cancer Institute, Navy Medical Oncology Branch, Naval Hospital Bethesda, USA.

Utilizing the whole‐cell patch‐clamp method we assessed the Ca2+current (Ica) in well‐established cell lines from human small‐cell carcinoma (SCC) of the lung, NCI‐H209 and NCI‐H187. The Ca2+current was readily observed in H209 tumour cells (90% of the cells tested), whereas H187 tumour cells only occasionally expressed Caz+channels (26% of the cells tested). H209 Ca2+current was evoked by potentials greater than ‐30 mV and exhibited partial inactivation over the duration of a 40 ms command potential. This inward current was unchanged by alteration of the holding potential from ‐ 80 to ‐ 40 mV and the activation phase of the Ca2+current was best fitted by Hodgkin‐Huxleym(t)2kinetics. H209 Ca2+current was reduced over 80% by verapamil (100 μM), whereas w‐conotoxin (5 μM) appeared to be without effect. In contrast, H209 Ca2+current was rapidly abolished by nifedipine (10 μm), strongly suggesting the presence of L‐type Ca2+channels. Voltage‐gated Ca2+channels may be important to the secretion of ectopic hormones and the etiology and pathogenesis of Lambert‐Eaton syndrome, an autoimmune disorder of the motor nerve terminal in which autoantibodies directed against voltage‐gated Ca2+channels are produced.
Characterization of the antisecretory action of prostaglandin D2in the rat colon
Authors: DIENER M. , NOBLES M. , SCHMITT C. , RUMMEL W.
Published: December 2008

Previous studies have shown that prostaglandin D2(PGD2) inhibits neuronally mediated secretion in the rat colon. This antisecretory action of PGD2was further characterized by the use of a prostaglandin D receptor blocker. Prostaglandin D2inhibited the neuronally mediated short‐circuit current evoked by prostaglandin I2, which represents Cl‐secretion. The concentration‐response curve for the inhibition by PGD2was shifted to the right in the presence of the prostaglandin D receptor blocker, AH 6809. AH 6809 had no effect on the short‐circuit current response induced by prostaglandin E2or iloprost, a stable prostaglandin I2analogue, suggesting an interaction of the blocker with receptors specific for PGD2.

A direct interaction of PGD2with enteric neurones was studied by determining its effect on acetylcholine release from enteric neurones preloaded with [3H]choline. Prostaglandin D2suppressed3H release induced by electric field stimulation. It had, however, no effect on the release induced by depolarization with potassium. The results suggest that the inhibitory action of PGD2on enteric cholinergic neurones is mediated by prostaglandin D receptors.
Cardiovascular and renal effects of intracerebroventricular angiotensin II in conscious sheep
Authors: HJELMQVIST H. , ULLMAN J. , HAMBERGER B. , RUNDGREN M.
Published: December 2008

Effects on systemic and pulmonary haemodynamics, renal electrolyte excretion, and plasma concentration of vasopressin, catecholamines, electrolytes and proteins in response to intracerebroventricular infusions of [Val5]‐angiotensin II (ANG II) at 1, 2 and 4 pmol kg‐1min‐1in isotonic saline for 30 min were studied in conscious sheep (n = 6). Vehicle control infusions were performed in four of the animals. All three doses of ANG II were expected to increase CFS concentration of the peptide above physiological levels. All ANG II infusions were noticed to be dipsogenic, but the animals were not allowed to drink freely until at the end of the experiments (at 120 min post‐infusion).

The systemic arterial blood pressure increased significantly only in response to 2 and 4 pmol kg‐1min‐1, concomitant with an increase of the systemic vascular resistance, whereas the cardiac output and heart rate remained unchanged. The central venous pressure increased only after administration of the highest ANG II dose, while pulmonary artery, and capillary wedge pressures were unaffected during all experiments.

The plasma protein and K concentration fell in response to ANG II administration. Also here, the effects were significant only at 2 and 4 pmol kg‐1min‐1. The plasma levels of vasopressin, noradrenaline, adrenaline and dopamine did not change significantly in response to any of the infusions.

The renal Na excretion increased by 100–400%, but not in a strictly dose‐dependent manner. Much smaller and more variable effects were seen on the renal K excretion.

We conclude that: (1) supraphysiological CSF ANG II levels are needed to cause a pressor effect when the peptide is administered via the intracerebroventricular route in conscious sheep; (2) the blood pressure is increased exclusively via peripheral vasoconstriction and; (3) increased vasopressin release does not contribute to the cardiovascular changes. The results also demonstrate that ANG II may cause haemodilution via a central site of action.
Pavlovian conditioning of corticotropin‐releasing factor‐induced increase of blood pressure and corticosterone secretion in the rat
Authors: KREUTZ M. , HELLHAMMER D. , MURISON R. , VETTER H. , KRAUSE U. , LEHNERT H.
Published: December 2008

Corticotropin‐releasing factor (CRF) is clearly involved in the central regulation of the pituitary‐adrenal axis and, moreover, of autonomic nervous system functions. Enhanced sympathetic activity with subsequent increases in blood pressure and heart rate and attenuation of the baroreceptor reflex results from the intracerebroventricular (i.c.v.) administration of CRF. Additionally, the peptide has a variety of potent effects on behavioural responses in animals similar to those observed after an experimentally evoked stress. It was therefore of obvious interest to examine whether CRF is a possible mediator of the learning processes associated with physiological stress reaction patterns. This report clearly demonstrates a classical conditioning of the endocrine (i.e. corticosterone secretion) and haemodynamic (i.e. blood pressure) sequelae following central CRF application and thus indicates that this mechanism is of physiological significance for learned stress responses.
Muscle samples obtained by needle biopsy are suitable for studying single fibre contractile properties
Authors: LYNCH G. S. , STEPHENSON D. G. , WILLIAMS D. A.
Published: December 2008

Recent speculation as to whether material obtained by needle biopsy can be used to study physiological properties of single muscle fibres, led us to investigate whether fibre segments obtained by this procedure, exhibit the same contractile characteristics as those fibre segments obtained from ablated whole muscles. Needle biopsies were taken of the upper hindlimb from adult, Sprague‐Dawley rats, killed by diethyl ether overdose. Single muscle fibre segments were isolated by microdissection, mechanically skinned (sarcolemma removed) and attached to a sensitive force recording transducer to measure Ca2+‐ and Sr2+‐activated responses. No significant differences were found in Ca2+‐ and Sr2+‐activated contractile characteristics (including maximum force generation) between fibres sampled by needle biopsy and those dissected from ablated intact muscles. Needle biopsied muscle fibre segments maintained their characteristic properties for up to 6–8 h (after sampling) if kept at room temperature in paraffin oil, and for up to 36 h if refrigerated (2–5 °C) in paraffin oil immediately after the biopsy procedure. It is concluded that muscle fibres sampled by needle biopsy have similar properties to fibres isolated from ablated muscles.
Effects of polyamines on intracellular calcium and mechanical activity in smooth muscle of guinea‐pig taenia coli
Authors: NILSSON B.‐O. , STRAND P. HELL
Published: December 2008

The effects of the polyamines putrescine, spermidine and spermine on the mechanical activity in smooth muscle from guinea‐pig taenia coli were investigated. Tissue concentrations of spermidine and spermine were about 240 and 160 nmol g‐1, respectively, while the putrescine concentration was much lower (4 nmol g‐1). Intracellular [Ca2+] was determined using the Fura‐2 method and the effects of extracellularly applied polyamines were observed. Spermine (10‐5–10‐3mol l‐1) dose‐dependently inhibited spontaneous contractions as well as contractions induced by 20–25 mmol l‐1KCl, with 10‐3mol l‐1spermine giving nearly total relaxation. Spermidine (10‐3mol l‐1) relaxed a 20 mmol l‐1KCl contracture, while putrescine had no effect. A decrease in intracellular [Ca2+] accompanied the relaxation induced by spermine. In contrast to the effects on spontaneous activity and intermediate [KCl], both the contraction and the accompanying increase in intracellular [Ca2+] induced by 90–120 mmol l‐1KCl were unaffected by spermine. Spermine did not affect the maximal Ca2+‐induced force of chemically skinned taenia coli preparations, but a small potentiating effect on the Ca2+sensitivity was observed. The results indicate that the relaxation induced by spermine depends on an intact cell membrane. Furthermore, the relaxing effect is due to decreased intracellular [Ca2+] and seems to occur only when the contraction is elicited by repetitive action potentials, and not by sustained depolarization.
Plasma potassium concentration as a determinant of proximal tubular NaCl and NaHCO3reabsorption in dog kidneys
Authors: STOKKE E. S. , NdÆSS P. A. , ØSTENSEN J. , LANGBERG H. C. , KIIL F.
Published: December 2008

To examine whether an acute increase in plasma potassium concentration ([K]p) may inhibit proximal tubular transport, clearance studies were performed in seven anaesthetized, volume expanded dogs treated with amiloride (1 mg kg‐1body wt) to block tubular potassium secretion, and with bumetanide (30μg kg‐1body wt) to inhibit NaCl reabsorption in Henle's loop. As [K]pwas raised in steps from 2.6 ± 0.2 to 7.9 ± 0.2 mm, bicarbonate, chloride, and sodium reabsorption decreased by 232 ± 56, 520 ± 59 and 958 ± 112μmol min‐1, respectively, at constant glomerular filtration rate (GFR). On average, the molar ratio between the inhibitory effects on bicarbonate and chloride reabsorption were 1:2.2–2.4. Reabsorption was calculated at GFR 100 ml min‐1: (reabsorption 100/GFR (mmol min‐1). It was inversely correlated to In [K]pwith r=–0.82 for bicarbonate and with r =–0.89 for chloride. Fractional potassium reabsorption remained constant at 0.31 ± 0.03. Administration of acetazolamide (100 mg kg‐1body wt) in eight dogs at [K]p8 mmreduced fractional reabsorption of bicarbonate, chloride and sodium as much as in previous studies on normokalaemic dogs. We conclude that acute elevation of [K]pinhibits NaHCO3transport and passive proximal tubular NaCl reabsorption. This inhibition is not related to changes in potassium secretion and carbonic anhydrase activity, but may be secondary to depolarization of the basolateral membrane.
Resetting of tubuloglomerular feedback by interrupting early distal flow
Authors: MORSING P. , VELAZQUEZ H. , ELLISON D. , WRIGHT F. S.
Published: December 2008

Cell–cell contact between the macula densa and the glomerular arterioles is thought to provide the information pathway for the tubuloglomerular feedback (TGF) mechanism. When concentrations of sodium and chloride in the macula densa segment are increased, a signal is transmitted through the extraglomerular mesangium to contract the afferent arteriole. In addition, some observers have described a second region of contact between a later part of the distal tubule and the afferent arteriole of the same nephron. In this region the connecting tubule (CNT), and sometimes nerves that make contact with the cells of this CNT, were found. This arrangement gives another potential tubular segment, besides the macula densa plaque, in which the composition of tubular fluid may regulate glomerular dynamics.

The present study was designed to investigate whether interrupting flow in the distal tubule downstream from the macula densa would influence the TGF mechanism. TGF was examined in rats by orthograde microperfusion, before and after blockade of the distal nephron with castor oil. Two variables were measured: maximum decrease in stop‐flow pressure (ΔPsf), and perfusion rate which elicits half‐maximal decrease in ΔPaf (V1/2). The fluid arriving at the blocking point was collected into a micro‐pipette. The results show a significant increase in V1/2 from 19 to 25 nl min‐1after 30 min of blockade. In conclusion the results support a role of the distal nephron in the control of the TGF mechanism.
Cardiovascular changes during an isometric contraction combined to a cold pressor test
Authors: KAHN J.‐F. , PITON A. , LEPAGE S. , BRUNET A. , LAGHA A. , MONOD H.
Published: December 2008

Fifteen normotensive male subjects (age, 27.9±1.3 years) performed isometric contractions (handgrip) at 15, 30 and 50% maximal voluntary contraction respectively for 7, 3 and 1 min. The contractions were sustained with or without a cold pressor test of the same duration (immersion of one foot in water of 5.2 ± 0.1oC). At rest, under the influence of a cold pressor test for 3 min, the heart rate increased from 74.3 ± 2.2 to 83.3 ±2.1 beats min‐1 (P < 0.001) in less than 10 s, and returned to the control value in 3 min; on the contrary, at the end of 3 min of cold pressor test, the systolic blood pressure was still above the control value (135.5 ± 4.2 and 121.0 ± 3.2 mmHg, P < 0.001). During the contractions, there was no significant difference between heart rate and systolic blood pressure values obtained with or without cold pressor test. Similarly, there was no significant change in the concentrations of plasma catecholamines. This absence of cardiovascular effect of cold pressor test associated with isometric contraction (for three relative force levels) is probably due to the increasing importance of sympathetic cardiac activation produced by the contraction with respect to that produced by the cold pressor test, the absence of supplementary changes in total peripheral resistance and a partial reciprocal inhibition of pain produced by the simultaneous performance of these two tests.
Potentiation of serotonin‐induced contractility of gastric fundus strips in lactating rats
Authors: DESHPANDE S. B.
Published: December 2008

Gastric fundus strips isolated from lactating, non‐lactating and pregnant rats were used to obtain agonist‐induced contractionsin vitroand the mechanism of alteration in gastric contractility to serotonin during lactation was investigated. The gastric contractile responses to 5‐HT expressed as area per unit mass of muscle (cm2g‐1muscle) were 60–65 % greater in lactating rats compared with non‐lactating rats. However, responses evoked by acetylcholine (ACh) or histamine were not different. The EC50values for 5‐HT were not different in either group indicating that there was no alteration in the 5‐HT affinity for its receptors in lactating rats. In pregnant rats, 5‐HT‐induced gastric responses were significantly (P <0.05) lower than those of non‐lactating rats. Pre‐treatment of non‐lactating rats with haloperidol (which increases plasma prolactin levels) enchanced the gastric contractile response to 5‐HT (P <0.05). On the other hand bromocriptine administration (which lowers plasma prolactin levels) in lactating or immature rats, decreased the contractile response to 5‐HT significantly, while bath application of bromocriptine (0.1 μM) had no effect. Incubation of fundus strips in physiological solution containing prolactin (10 μg ml‐1) for 24 h decreased the 5‐HT evoked contractions, but not the ACh evoked responses. The results in this study indicate that prolactin modulates the intrinsic contractile activity of the gastric smooth muscles to 5‐HT.
Measurements of duodenal wall motility, mucosal fluid transport and alkaline secretion. Description and evaluation of a methodological approach in the anaesthetized cat
Authors: FÄNDRIKS L.
Published: December 2008

This paper describes and evaluates a method for simultaneous recordings of duodenal motility and mucosal secretions in chloralose‐anaesthetized cats. Biliary and pancreatic secretions were diverted by separate cannulation of each duct. A 2 cm segment of the proximal duodenum was isolated between two luminally situated balloons (the proximal balloon being positioned immediately distal to the pylorus). Each balloon was connected to a barostatic device maintaining a constant pressure within the balloon independent of the degree of contraction. Motor activity in the duodenal wall was recorded as changes in balloon volume. The duodenal segment was perfused at a constant rate with isotonic saline containing [14C]PEG 4000 as a non‐absorbable marker. The recovered perfusate was sampled in 5 min fractions and analysed with regard to alkalinity (back titration) and concentration of marker (liquid scintillation). Net alkalinization and net fluid transport was calculated with conventional equations. The sensitivity of the analytical procedures was tested bench‐side. The technique was evaluated in vivo during basal conditions and during acid exposure of the mucosa. Exposing the duodenal segment to 30 mM HC1 induced a marked change in the duodenal functional state with the occurrence of a polarized duodenal motility pattern, net fluid secretion and an increased alkaline secretion.
Tissue‐specific reduction of galanin content in the pancreas in alloxan diabetes in the mouse
Authors: DUNNING B. E. , AHRÉN B.
Published: December 2008

Galanin inhibits insulin secretion and has been proposed to function as a sympathetic neurotransmitter in the endocrine pancreas in some species, for example in the dog. In this study, pancreatic and adrenal gland galanin content were measured following experimental diabetes induced by alloxan in mice. Three days after administration of alloxan (70mgkg‐1, i.p.) in normal mice, pancreatic content of galanin‐like immunoreactivity (GLIR) was reduced to 65 ± 11 % of that in untreated controls (P< 0.01), whereas adrenal gland GLIR was unchanged. Similarly, 8 days after alloxan administration, pancreatic GLIR was reduced (P< 0.002), whereas adrenal gland GLIR was unaffected. Pancreatic GLIR also inversely correlated with plasma glucose levels (r = ‐0.5055,P< 0.005). To distinguish between the direct effects of alloxan vs. indirect metabolic effects induced by the drug, alloxan‐diabetic mice were treated with insulin twice daily, which normalized the plasma glucose levels (7.6 ± 0.3 mmol l‐1). Pancreatic GLIR was then not significantly different from controls. Thus pancreatic but not adrenal gland GLIR content is reduced in alloxan‐induced diabetes in mice. The data support a role for galanin as a pancreatic sympathetic neurotransmitter which may participate in the metabolic alterations seen in alloxan diabetes in mice.
Exogenous arachidonic acid inactivates protein kinase C in mouse pancreatic islets
Authors: THAMS P. , HEDESKOV C. J. , CAPITO K.
Published: December 2008

The effect of arachidonic acid on protein kinase C activity and insulin secretion in mouse islets was investigated. Arachidonic acid stimulated protein kinase C activity in islet cytosol and membrane fractions by substituting for phosphatidylserine. Stimulation by arachidonic acid was dependent on either Ca2+ or the phorbol ester 12‐O‐tetradecanoylphorbol 13‐acetate, was potentiated by the combined addition of Ca2++ 12‐O‐tetradecanoylphorbol 13‐acetate, and did not further increase protein kinase C activity in the presence of saturating concentrations of phosphatidylserine. Arachidonic acid stimulation of protein kinase C was prevented by binding of arachidonic acid to albumin.

In the absence of extracellular Ca2+, exogenous arachidonic acid stimulated insulin secretion. Arachidonic acid‐induced insulin secretion was not potentiated by 12‐O‐tetradecanoylphorbol 13‐acetate and was not prevented by the protein kinase C inhibitor staurosporine, suggesting that arachidonic acid‐induced insulin secretion may occur independently of protein kinase C activation. Arachidonic acid‐induced insulin secretion in Ca2+‐free medium was on the other hand potentiated by addition of extracellular Ca2+.

Stimulation of insulin secretion by exogenous arachidonic acid was associated with inactivation of protein kinase C. Inactivation of protein kinase C was also observed in islet homogenate after pre‐incubation with arachidonic acid. Arachidonic acid‐induced protein kinase C inactivation in islet homogenate was prevented by albumin or MgATP. Inactivation by arachidonic acid in intact islets was, however, not produced during enzyme isolation and was not prevented by inclusion of albumin or MgATP during preparation of protein kinase C extracts.

In conclusion, it is suggested, that arachidonic acid, by inactivating protein kinase C, may exert toxic effects in islets, and that arachidonic acid may stimulate insulin secretion by a non‐physiological mechanism, possibly involving an ionophoretic effect of arachidonic acid to induce Ca2+‐mediated insulin release.
Hyaluronan turnover in the rat small intestine
Authors: ØSTGAARD G. , REED R. K.
Published: December 2008

The main metabolic pathway for the interstitial matrix component hyaluronan seems to be via lymph. Present estimates of turnover of intestinal hyaluronan are based on isolated organs and/or experiments in anaesthesia over a few hours. In this study lymph was sampled from the main mesenteric lymphatic for 24 h in awake, restrained rats. The tissue content of hyaluronan averaged 28 /μ g‐1 in the duodenum/jejunum and 124 μ g‐1 in the colon. Based on tissue content and lymphatic output, the turnover rate of hyaluronan in the small intestine was estimated at approximately 50%. In another experimental group anaesthetized rats were fed either phosphate buffer or triolein in buffer via a gastric tube. Lymph flow increased with fluid absorption from the gut and hyaluronan output in lymph was elevated correspondingly. However, no effect of acute fat administration on hyaluronan concentration or lymph flow could be demonstrated.
Enhanced heart rate response to haemorrhage by ileus in the pig
Authors: JACOBSEN J. , HANSEN O. B. , SZTUK F. , WARBERG J. , KNIGGE U. , SECHER N. H.
Published: December 2008

Effects of ileus on cardiovascular and hormonal responses to haemorrhage were evaluated in 10 anaesthetized pigs. Ileus was induced and the bleeding sequence repeated on the following day. Before ileus, a resting heart rate (HR) of 105 (range 83–140) beats min‐1 remained unchanged until haemorrhage amounted to 15% of the blood volume. With a blood loss of 28% HR increased to a maximum of 162 (126–245) beats min‐1. In contrast, ileus increased HR upon initiation of haemorrhage from a similar resting value to a maximum of 200 (152–250) beats min“1 (P < 0.0005). There were neither statistical differences in mean arterial pressure, cardiac output, central venous pressure, thoracic electrical impedance, pulmonary arterial mean pressure, pulmonary wedge pressure, pulmonary and systemic vascular resistances, nor in plasma concentrations of dopamine, adrenaline, vasopressin and aldosterone during haemorrhage before and after ileus. Plasma noradrenaline increased more with haemorrhage after than before ileus: from 2.8 (1.2–5.0) to 13 (2.3–59.0) vs. 3.0 (1.5.2) to 3.6 (2.7–17.5) nmol l”1 (P < 0.005). Also, the pancreatic polypeptide response to haemorrhage was enlarged with ileus (29 (0–60) to 90 (45–145) vs. 23 (0–64) to 57 (27–106) pmol l“1 (P < 0.005)). No significant differences could be detected in cardiovascular and hormonal responses to haemorrhage before and after a sham‐operation in three pigs. Results demonstrate an immediate and enhanced HR response to haemorrhage in the pig with ileus, reflected in sympathetic activation as indicated by plasma noradrenaline.
Myocardial oxygen supply and lactate metabolism during marked arterial hypoxaemia
Authors: GRUBBSTRÖM J. , BERGLUND B. , KAIJSER L.
Published: December 2008

Myocardial O2 delivery and changes in myocardial lactate metabolism during marked hypoxaemia (pao2 5‐5.4 kPa, Sa O2 70–75%) produced by 12% O2 breathing were studied in 12 healthy subjects at rest and during supine exercise up to maximal intensity. Blood for O2 and lactate analyses was sampled from catheters in an artery (a) and the coronary sinus (cs) and coronary sinus blood flow (CSBF) was measured by thermodilution. Lactate metabolism was evaluated in a subgroup of the subjects using i.v. infusion of [14C]lactate.

At rest and during submaximal exercise up to heart rate 156 beats min‐1 myocardial O2 uptake (MQO2) was maintained at the same level during hypoxaemia as during normoxaemia. This was achieved at rest mainly by a more complete O2 extraction, during exercise entirely by greater CSBF. During maximal exercise CSBF was 35% greater during hypoxaemia than normoxaemia, while there was no difference in cs O2 saturation. Maximal MQO2 was smaller during hypoxaemia than normoxaemia in spite of no difference in rate pressure product. The a‐cs difference of lactate was reduced during hypoxaemia and there was a significant myocardial release of lactate, as calculated from [14C]lactate data, during hypoxaemic exercise, but not during hypoxaemic rest or normoxaemic rest and exercise. It is concluded that the heart has a coronary flow reserve of about 35%, which can be utilised under hypoxaemia. When this reserve is insufficient to supply the myocardium with oxygen lactate is produced to cover part of the myocardial ATP regeneration.
The effect of experimental frost‐bite on the responses of the rabbit ear‐artery to adrenergic and electrical stimulation
Authors: ØSTNES J.E. , AAS P.
Published: December 2008

The aim of the present investigation was to study the effect of sub‐zero temperatures on the adrenergic activated, smooth muscle‐contraction of a peripheral blood‐vessel. The central ear‐artery of the rabbit was used for this purpose. The artery was stimulated to contractin vitroby activation of phentolamine sensitive, post‐junctional, a‐adrenoceptors by use of noradrenaline, or by noradrenaline released from noradrenergic nerves in the blood‐vessel following electrical field stimulation. The effect of freezing the tissuein vivofor 15 min at sub‐zero temperatures (–4, ‐ 6 and – 9oC) was studiedin vitro.Exposure to – 4 and – 6oC did not alter the apparent affinity (ED60) of noradrenaline significantly, when measured immediately, or 2 or 6 days after exposure. The maximal response to noradrenaline was reduced by approximately 54, 74 and 100% following exposure to –4, – 6 and – 9oC, respectively. The response was completely restored after 2 and 6 days of regenerationin vivofollowing exposure to – 6oC, whereas the response after exposure to – 9oC was restored by only about 8 and 30% after 2 and 6 days regeneration, respectively. The maximal response to electrical field stimulation, which was completely inhibited by tetrodotoxin and phentolamine, was reduced by approximately 92% after exposure for 15 min to –4 and – 6oC, while it was completely inhibited after exposure to – 9oC. The response was restored by only 15–20% following 2 and 6 daysin vivoafter exposure to – 6oC. No regeneration of the contraction induced by the electrical stimulation was observed after 2 or 6 days following exposure to –9oC. The results of the present study suggest that noradrenergic nerves in the central ear‐artery of the rabbit are more sensitive to subzero temperatures than are the post‐junctional, noradrenergic α‐receptors and the smooth muscle of the blood‐vessel. The damage induced by freezing appeared to be both time and temperature dependent and there was only limited restoration of the nervous function 6 days after severe freezing.
Effect of endothelium‐derived relaxing factor on renin secretion from isolated mouse renal juxtaglomerular cells
Authors: SCHRICKER K. , RITTHALER T. , KRÄMER B. K. , KURTZ A.
Published: December 2008

This study aimed to examine the direct influence of native endothelium derived relaxing factor (EDRF) on renin secretion. To this end isolated mouse renal juxtaglomerular cells were cocultured with bovine aortic endothelial cells which produced and released significant amounts of EDRF as assayed by guanylate cyclase activities which were measured separately in endothelial and juxtaglomerular cells as well as in the cocultures of juxtaglomerular with endothelial cells. EDRF production was blunted in the absence of extracellular L‐arginine and in the presence of Nw‐nitro‐L‐arginine (L‐NAG; 200 μM).

Inhibition of endothelial EDRF production by removal of arginine or addition of L‐NAG was associated with a significant decrease of renin secretion from the cocultures while the same regimen had no effect on renin secretion from JG cells alone. Exogeneous generation of nitric oxide by the addition of sodium nitroprusside (100 μM) stimulated renin secretion in the cocultures both at normal and inhibited EDRF formation as well as from juxtaglomerular cells alone.

These findings suggest that native EDRF released from vascular endothelial cells is a stimulatory signal for renin secretion from renal juxtaglomerular cells.
Osmotic barrier properties of the rat peritoneal membrane
Authors: ZAKARIA E. R. , RIPPE B.
Published: December 2008

In this study the osmotic barrier characteristics of the rat peritoneal membrane were investigated. Fluid movements between the peritoneal cavity and the blood were measured following instillation of isotonic saline (control) and hypertonic solutions of NaCl, glucose, sucrose, raffinose and myoglobin (test solutions). Moreover, 5 and 8% albumin in NaCl were investigated. Osmotic transients were assessed using a simple volume recovery technique. Peritoneal osmotic conductances (i.e. products of peritoneal hydraulic conductances [LPS] and solute reflection coefficients [s̀]) were calculated from the differences in the rates of peritoneal fluid loss and in osmotic pressures between test solutions and the isotonic saline control solution. The osmotic conductance to glucose was estimated to be 1.63/l min‐1 mmHg‐1 m‐2 and that for albumin to be 59.6 μl min‐1 mmHg‐1 m‐2. Assuming an albumin s̀ of 0.9, the s̀ of glucose was estimated to be 0.025, in accordance with previous measurements for the cat peritoneal membrane. The osmotic conductances assessed here were compatible with an overalľ peritoneal equivalent small pore radius of 47–48 Å, but could also be fitted to a three‐pore model of peritoneal permselectivity, including a transcellular (ultra‐small pore) pathway and a large pore pathway. The great discrepancy between peritoneal s̀ for small solutes and that for albumin obtained in this study indicates that small solute reflection coefficients are close to zero while that for albumin is not far from unity. Furthermore, the peritoneal hydraulic conductance (ultrafiltration coefficient) is large enough to allow for a substantial absorption of fluid directly into the plasma when the crystalloid osmotic pressures in blood and peritoneal dialysate are in equilibrium.
Effects of chloride transport inhibitors on intestinal fluid and ion transport in vivo and in vitro
Authors: FRYKLUND J. , MATTSSON J. P. , BERGLUND M.‐L. , HELANDER H. F. , LARSSON H.
Published: December 2008

The hypothesis that intestinal fluid secretion is driven by Cl‐ has been tested by investigating the effects of NPPB (5‐nitro‐2‐(3‐phenyl‐propylamino)‐benzoate), a blocker of Cl‐ channels in nephrons, and the loop diuretic bumetanide, an inhibitor of the Na+, K+, 2 Cl‐‐co‐transporter. Both NPPB (IC50 (inhibitory concentration) ∼ 100 μM) and bumetanide (IC50∼μM) inhibited stimulated short‐circuit current (Isc) in monolayers of a colonic cell line T84. NPPB also inhibited 3aCl‐ uptake by these cells, indicating that NPPB acts as a CI‐ channel blocker in the T84 cells. NPPB (300μM) and bumetanide (10 μM) abolished both stimulated /sc and CI‐ secretion in isolated rat colonic mucosa. As judged by autoradiography, [3H]NPPB was found both in the crypts and at the surface after exposure of either side to the compound. In line with these results, NPPB and bumetanide reduced stimulated fluid secretion in everted colon sacs from the rat. In the anaesthetized rat model, neither bumetanide nor NPPB affected the net fluid transport. After luminal administration of [3H]NPPB to the rat, radioactivity was found mainly in the villus tips, whereas no labelling was found in the crypts. NPPB was bound to plasma protein (99%), and the inhibitory effects of both NPPB and bumetanide on Isc in T84 cells and fluid secretion in the colonic sacs decreased in the presence of albumin, again indicating that the compounds might not reach the in vivo target, or that the mechanism for fluid secretion in vivo may not be explained solely by the secretion of CI‐
Increased insulin‐stimulated glucose uptake in athletes: the importance of GLUT4 mRNA, GLUT4 protein and fibre type composition of skeletal muscle
Authors: ANDERSEN P. H. , LUND S. , SCHMITZ O. , JUNKER S. , KAHN B. B. , PEDERSEN O.
Published: December 2008

In the present study the expression of GLUT4 and fibre type composition were examined in biopsies from skeletal muscle in seven male athletes and eight male sedentary subjects. Estimated maximal oxygen uptake was increased in the trained group when compared with the sedentary group (74.0 ± 3.9 vs. 42.9±5.1 ml kg‐1 min‐1; P < 0.01). A biopsy of vastus lateralis muscle was taken in the fasting state, 36 h after the last bout of exercise. A second muscle biopsy was obtained following 4 h of a hyperinsulinaemic (2 mU kg‐1 min‐1), euglycaemic clamp. The rate of insulin‐stimulated glucose uptake was increased in the trained subjects (17.34±0.53 vs. 13.53±0.79 mg kg‐1 min‐1, P < 0.01). In parallel, the steady state levels of GLUT4 protein and mRNA per DNA were higher in muscle biopsies obtained in the basal state from athletes than in sedentary controls, 21 and 71% respectively (P < 0.05). In the total group of participants, GLUT4 protein per DNA in the basal state and insulin‐stimulated glucose uptake rate correlated positively, (r = 0.51, P = 0.05). In the insulin‐stimulated state we did not find any significant correlation between GLUT4 protein per DNA and glucose uptake rate (r = 0.13, n.s.). No significant relationships between GLUT4 protein abundance per DNA and muscle fibre type distribution were observed. A significantly negative correladon was found between type 2B fibre area and insulin‐stimulated glucose uptake (r =–0.63, P < 0.05). In conclusion, the abundance of GLUT4 protein and mRNA, respectively, is increased in skeletal muscle from endurance trained subjects compared to sedentary subjects. However, factors other than GLUT4 immunoreactive protein abundance seem to be determinant for the increased insulin‐stimulated whole body glucose uptake in endurance trained subjects.