bluuebunny/crossref_metadata_2025_split huggingface dataset:
Plasma immunoreactive atrial natriuretic peptide and vasopressin after ethanol intake in man
Authors: LEPPÄLUOTO J. , VUOLTEENAHO O. , ARJAMAA O. , RUSKOAHO H. 
Published: December 2008

To study the mechanisms of alcohol‐induced diuresis, the plasma concentration of immunoreactive atrial natriuretic peptide and arginine vasopressin, serum sodium and osmolality, plasma renin activity and aldosterone, urinary sodium and volume, free water clearance, blood pressure and heart rate were measured in seven healthy men after oral intake of ethanol (1.5 g kg‐1 in 6 h). Serum ethanol levels increased to 27 ± 4 mmol 1‐l (mean ± SD) in 30 min and remained detectable for 14 h. Serum osmolality rose from 280±10 to 340 ± 4 mosm kg‐1 in 2 hours (P < 0.01) and was 300 ± 4 at 14 h (P < 0.01). Formation of hypotonic urine began after the alcohol intake and resulted in a net loss of 0.9 ± 0.1 kg water in 2 h. Free water clearance increased from ‐3.4 ± 1.4 to 2.8 ± 1.5ml min‐l in 2 h (P < 0.01). Plasma immunoreactive arginine vasopressin decreased from 5.7 ± 2.1 to 3.3 ± 1.3 ng 1‐1 (P = 0.05) in 30 min and increased to 17 ± 25 and 12±10 ng 1‐1 at 6 and 12 h, respectively (P < 0.05 for both). Plasma immunoreactive atrial natriuretic peptide levels decreased from 17 ± 9 to the minimum of 11 ± 3 ng 1‐1 in 2 h (P < 0.01) and returned to the initial levels in 6 h. Serum sodium, plasma renin activity and plasma aldosterone increased maximally by 4 ±2, 165 ± 153 and 143 ± 101 % (P < 0.01 each) during 1–6 h. No changes in blood pressure were observed during the ingestion period, but the heart rate rose significantly from 70 min‐1 at 6 p.m. to 95 min‐1 at 12 p.m.We conclude that ethanol intake in relation to serum ethanol levels caused in the first phase a rapid increase in osmolality which was associated with a decrease in plasma immunoreactive arginine vasopressin. This caused hypotonic diuresis and increased free water clearance followed by volume contraction which evidently led to decreased plasma immunoreactive atrial natriuretic peptide. Serum osmolality was significantly elevated during the whole experiment and serum sodium 1–2 h after the ethanol intake. This was associated with the return of plasma immunoreactive atrial natriuretic peptide to initial levels after 6 h, the increase in plasma immunoreactive arginine vasopressin levels and reduced diuresis after 2 h. Our results suggest that ANP is not responsible for the diuresis seen after the alcohol intake.
Human, tactile, directional sensibility and its peripheral origins
Authors: NORRSELL U. , OLAUSSON H. 
Published: December 2008

Tactile directional sensibility is probably functionally important and deserves attention as it is known to be sensitive to many different disturbances of the somatosensory system. Therefore, the ability of healthy adults to determine the direction of motion of a light tactile stimulus travelling proximally or distally along a straight line on depilated, hairy skin of the forearm was examined with two‐alternative, forced‐choice technique. The aim was to investigate the relative importance of different types of afferent information which may be used for this purpose. A test was started with the moving stimulus covering a distance of no less than 2.5 mm, which was subsequently increased until the subject could report the direction of motion reliably.Afterwards, the distance was decreased until the subject could no longer do so. Three different stimulation conditions were used and for a point stimulator touching the skin it was found that the necessary distance decreased to 2.5 mm after a moderate increase of the vertical contact load. No such decrease was found when a frictionless air‐stream point stimulator was used instead. The distances which had to be covered by the point stimulator touching the skin increased to values which were comparable to those obtained with the air‐stream stimulator after the lateral extensibility of the skin had been diminished. This was achieved by attaching a surgical sticky plaster around the stimulated skip area. The present findings consequently indicated that optimal, tactile, directional sensitivity depends on peripheral afferent messages which signal the direction of lateral stretching of the skin.
Selective inhibition by dactinomycin of NANC sensory bronchoconstriction and [125I] NKA binding due to NK‐2 receptor antagonism
Authors: LOU Y.‐P. , DELAY‐GOYET P. , LUNDBERG J. M. 
Published: December 2008

Y.‐P. Lou, P. Delay‐Goyet& J. M. Lundberg. 1991. Selective inhibition by dactinomycin of NANC sensory bronchoconstriction and [125I]NKA binding due to NK‐2 receptor antagonism.Acta Physiol Scand144, 221–231. Received 6 May 1991, accepted 13 September 1991. ISSN 0001–6772. Department of Pharmacology, Karolinska Institutet, Stockholm.In the present study, dactinomycin (m)inhibited the non‐adrenergic, non‐cholinergic bronchoconstriction upon antidromic vagal nerve stimulation (1 Hz for 1 min) in the isolated perfused guinea‐pig lung by 84%. The release of calcitonin gene‐related peptide was unchanged, however, suggesting a postjunctional action. Dactinomycin (10‐5, 5 × 10‐5m)also reduced non‐adrenergic non‐cholinergic bronchial contractions (maximally by 75%) induced by electrical field stimulation or capsaicin, while the cholinergic component and non‐adrenergic non‐cholinergic relaxation remained intact. The neurokinin‐2 receptor antagonist l‐659 877(10‐6m)had a similar effect as dactinomycin, inhibiting the non‐adrenergic non‐cholinergic bronchial contractions by 69%, while the neurokinin‐1 receptor antagonist CP‐96,345 (10‐6m)had no effect. The bronchoconstriction evoked by neurokinin A, the selective neurokinin‐2 receptor agonist Nle10neurokinin A (4–10) and capsaicin was markedly inhibited by dactinomycin while the contraction induced by substance P (SP), the selective neurokinin‐1 receptor agonist Sar9Met(02)11SP, endothelin‐1 and acetyl‐choline was not affected. In autoradiographic experiments on guinea‐pig lung, [125I]neurokinin A‐labelled sections showed dense binding in the bronchial smooth muscle layer. Dactinomycin inhibited the specific binding of [251]neurokinin A in a concentration‐dependent manner (IC50= 6.3 × 10‐6m)and 66% of [125I]neurokinin A total binding was inhibited by 10‐4M dactinomycin. In the rat colon, [125I]neurokinin A binding to neurokinin‐2 sites on circular smooth muscle was inhibited by dactinomycin with an IC50value of 7.9 × 10‐6M. Dactinomycin failed to reduce increased nerve‐evoked contractions or those caused by Nle10neurokinin A (4–10)per sein the rat vas deferens, which are considered to be mediated by neurokinin‐2 receptor activation. In the rat portal vein, dactinomycin did not influence the contractions caused by the neurokinin‐3 selective agonist Pro7neurokinin B. In conclusion, dactinomycin selectively inhibited neurokinin‐2 receptor activation in guinea‐pig lung and rat colon, but not in rat vas deferens, which may depend on the existence of different neurokinin‐2 receptor subtypes. Neurokinin A is most likely the main endogenous excitatory non‐adrenergic non‐cholinergic transmitter in guinea‐pig bronchi.
Alpha2‐receptor‐mediated inhibition of intraluminal release of gastric somatostatin in anaesthetized rats
Authors: ALIÑO S. F. , GARCIA D. , UVNÄS‐MOBERG K. 
Published: December 2008

Aliño, S. F., Garcia, D. & Uvnäs‐Moberg, K. 1992. Alpha2‐receptor‐mediated inhibition of intraluminal release of gastric somatostatin in anaesthetized rats.Acta Physiol Scand144, 233–238. Received 22 February 1991, accepted 11 October 1991. ISSN 00014772. Department of Pharmacology and Pharmaceutics, University of Valencia, Valencia, Spain, Department of Cell Biology and Morphology Science, University of Pais Vasco, Leioa, Spain and Department of Pharmacology, Karolinska Institute, Stockholm, Sweden.The aim of the present study was to investigate how the sympathetic nervous system affects the vagally induced intragastric release of somatostatin and gastrin. Experiments were performed on anaesthetized rats in which the stomach was perfused with a dextrane solution (pH ≅ 5.9) or dextrane buffer (pH 7.4). pH as well as gastrin and somatostatin levels were measured in the gastric perfusate when it had passed the stomach. Vagal stimulation caused a decrease in perfusate pH and an increase of the intraluminal output of gastrin and somatostatin when the stomach was perfused with the dextrane solution pH 5.9. Pretreatment with phentolamine (1 mg kg‐1) significantly increased and pretreatment with clonidine (60, ug kg‐1h‐1) significantly decreased somatostatin release caused by vagal stimulation, whereas gastrin levels remained largely unchanged. The effect of clonidine persisted in rats pretreated with indomethacin (5 mg kg‐1), whichper sepotentiates the vagally induced luminal somatostatin release. When the stomach was perfused with the dextrane buffer pH 7.4, basal gastrin levels were significantly higher than during perfusion with the solution pH 5.9, whereas somatostatin levels remained unchanged. Neither somatostatin nor gastrin levels increased following vagal stimulation during gastric perfusion with the dextrane buffer pH 7.4. However, following pretreatment with phentolamine somatostatin levels increased during these conditions.
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, DenmarkCardiopulmonary 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, SwedenWe 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.