Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Norepinephrine (0.35 microgram/kg/min) was infused continuously for 20 min into either the carotid, femoral or superior mesenteric arteries of anesthetized, vagotomized and splenectomized dogs. Blood flow in these arteries was monitored continuously. Blood samples were taken from the aorta, jugular or femoral vein and the superior mesenteric and hepatic veins at 5-min intervals during a 20-min preinfusion period, the 20-min infusion period and a 20-min postinfusion interval. Blood samples were analyzed by radioimmunoassay with antibodies raised against Leu- and Met-enkephalin. Norepinephrine infused into the carotid or femoral arteries did not affect plasma levels of enkephalin-like material. By contrast, plasma concentrations of both Leu- and Met-enkephalin-like material were more than doubled during norepinephrine infusion into the superior mesenteric artery, P less than .001. This increase in enkephalin-like material occurred in arterial as well as venous blood. Neither infusion of vasopressin nor prostaglandin F2 alpha into the superior mesenteric artery elicited a rise in plasma levels of enkephalin-like material. In adrenalectomized dogs, when norepinephrine was infused into the superior mesenteric artery, there was again a statistically significant elevation in plasma concentrations of both Leu- and Met-enkephalin-like material.
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PMID:Effect of norepinephrine on canine plasma concentrations of enkephalin-like material. 346 41

Increasing age impairs the regulation of blood pressure during posture change. The neuro-humoral and cardiovascular responses to head-up tilt were analysed in carefully-screened young and healthy elderly individuals. Mean blood pressure was significantly higher in the elderly but there were no differences in total peripheral resistance, heart rate, stroke volume and cardiac index. Age-related interactions were observed in the control of mean blood pressure, heart rate and stroke volume. Total peripheral resistance increased and cardiac index decreased but there was no difference in their control in the young and old. Noradrenaline, vasopressin, plasma renin activity and aldosterone all increased in response to the tilt. These observations indicate differences in the neuroendocrine responses and cardiovascular haemodynamics of young and old healthy individuals to head-up tilt and are particularly important because of all observations were made simultaneously in the same subject. It is suggested that a similar approach should be adopted in the investigation of patients with postural hypotension.
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PMID:Cardiovascular haemodynamics and the response of vasopressin, aldosterone, plasma renin activity and plasma catecholamines to head-up tilt in young and old healthy subjects. 351 87

Ten patients with advanced congestive heart failure were treated with an arginine vasopressin V1 antagonist during hemodynamic monitoring to determine the contribution of vasopressin to vasoconstriction in this disorder. The vasopressin antagonist caused a decrease in systemic vascular resistance in the three patients whose plasma vasopressin was greater than 4.0 pg/ml (average for the group was 2.4 +/- 0.6). Plasma vasopressin concentration correlated with the percent decrease of systemic vascular resistance (r = 0.70, p less than 0.025), serum sodium (r = 0.72, p less than 0.02) and serum creatinine (r = 0.85, p less than 0.005). To compare the relative roles of vasopressin, the renin-angiotensin system and the sympathetic nervous system, these patients also received captopril and phentolamine. Captopril decreased systemic vascular resistance by 20% (p less than 0.05), mostly in patients with high plasma renin activity. Levels of plasma renin activity ranged between 1 and 46 ng/ml per h (average 14.7 +/- 5.7) and correlated with serum sodium (r = 0.77, p less than 0.025), serum creatinine (r = 0.73, p less than 0.025) and right atrial pressure (r = 0.67, p less than 0.05). Phentolamine decreased systemic vascular resistance in all patients (average 34%, p less than 0.01), but the decrease did not correlate with the pretreatment norepinephrine concentration. Norepinephrine levels were elevated in all patients (694 +/- 110 pg/ml) and correlated with baseline stroke volume index (r = 0.75, p less than 0.025) and plasma renin activity (r = 0.67, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contribution of vasopressin to vasoconstriction in patients with congestive heart failure: comparison with the renin-angiotensin system and the sympathetic nervous system. 351 28

The development of shock initiates a cascade of responses in an effort to reestablish homeostasis. Three of the most important hormonal and neurohumoral changes are the secretion of glucocorticoids, catecholamines, and vasopressin. Regulation of adrenal function is much more complex than originally thought. Hemorrhage is a potent stimulus for cortisol release, and both ACTH and ACTH-independent mechanisms have been described. The ACTH response to its releasing hormone, corticotropin releasing hormone (CRF), is itself amplified by vasopressin, which appears to have intrinsic CRF properties. Because ACTH is synthesized as part of a large precursor molecule (pro-opiomelanocortin) containing the amino acid sequences for several important proteins, stimulation of ACTH release has far-ranging effects, the specifics of which are just being clarified. Norepinephrine and epinephrine levels increase manyfold above baseline within minutes of the onset of hemorrhagic shock. Only patients experiencing cardiac arrest or the rare patient with a very active pheochromocytoma have higher concentrations. The levels reached are far in excess of those required to cause both cardiovascular and metabolic alterations. Because of the presence of the endogenous opiates leucine and methionine enkephalin in the neurosecretory granule, it is very likely that the enkephalins are coreleased with the catecholamines, modifying their cardiovascular effects and producing analgesia. Hypovolemia is also a potent stimulus for vasopressin secretion, which overrides hypotonicity, presenting a clinical picture quite compatible with the syndrome of inappropriate antidiuretic hormone secretion, from which it must be differentiated. Vasopressin also is released by pain, nausea, and hypoxia, all of which are likely to be present in the patient with shock.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endocrinology of shock. 353 88

Noradrenaline (NA) (1-100 microM) was applied to 41 neurons recorded intracellularly from the supraoptic nucleus (SON) of the rat hypothalamic slice preparation; 34 (83%) neurons showed membrane depolarization which was dose-dependent. The depolarization was frequently accompanied by decreased membrane resistance, increased firing rate and increased fluctuations in membrane potential. Following the application of the alpha-agonist, phenylephrine, 10 out of 11 neurons tested showed similar responses, while the beta-agonist, isoproterenol, caused no changes in 6 out of 7 SON cells. We found no difference in responsiveness between neurons having a 'phasic' or a 'non-phasic' pattern of firing. We conclude that NA depolarized and increased the firing rate of both vasopressin- and oxytocin-containing neurons through an action on alpha-adrenergic receptors.
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PMID:Depolarizing effect of noradrenaline on neurons of the rat supraoptic nucleus in vitro. 356 13

The role of central adrenergic receptors in the control of vasopressin release was studied in the conscious rat. Norepinephrine (10 micrograms) and the alpha-1 agonist, phenylephrine (50 micrograms), administered intracerebroventricularly resulted in significant increases in the plasma vasopressin concentration and blood pressure. The alpha-2 agonist, BHT 933 (50 micrograms) and the beta agonist, isoproterenol (10 micrograms) both caused a significant decrease in the plasma vasopressin concentration with only small changes in blood pressure. The central administration of the alpha-1 antagonist corynanthine (20 micrograms) had no effect on the plasma vasopressin concentration; however, increases in plasma vasopressin levels were observed when either the alpha-2 antagonist yohimbine (20 micrograms) or the beta antagonist propranolol (20 micrograms) were given. It is concluded that central noradrenergic pathways may play an important role in the control of vasopressin release and that this control may involve alpha-1, alpha-2 and beta adrenoreceptors.
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PMID:Central adrenergic control of vasopressin release. 370 61

Circulatory changes and arterial plasma hormone concentrations were measured in seven healthy young adults during 30 and 60 degrees passive head-up tilt with the subjects supported by a saddle. The 30 degrees tilt induced a decrease in pulse pressure (Pp) from 45 +/- 2 to 35 +/- 4 (mean +/- SE) mmHg concomitant with an increase in heart rate (HR) from 58 +/- 4 to 78 +/- 8 beats/min and a marginal increase in mean arterial pressure (MAP). Norepinephrine increased from 180 +/- 20 to 310 +/- 40 pg/ml, aldosterone increased fivefold, and angiotensin II increased from 8 +/- 2 to 22 +/- 7 pg/ml. The 60 degrees tilt initially produced changes, which were qualitatively similar to the 30 degrees tilt. However, after 19 +/- 3 min sudden decreases were seen in MAP (94 +/- 3 to 50 +/- 8 mmHg), in Pp (38 +/- 5 to 18 +/- 4 mmHg), and in HR (90 +/- 7 to 57 +/- 6 beats/min). Concomitantly, epinephrine doubled while norepinephrine remained unchanged; the vagally controlled hormone pancreatic polypeptide increased from 29 +/- 3 to 51 +/- 8 pmol/l, vasopressin from 4 +/- 1 to 126 +/- 58 pg/ml, and angiotensin II from 23 +/- 9 to 35 +/- 12 pg/ml. The hypotensive bradycardiac episode was immediately reversible on termination of the head-up tilt.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypotension induced by passive head-up tilt: endocrine and circulatory mechanisms. 376 74

Small intramyometrial arteries and pieces of adjacent myometrial tissue were obtained from 25 non-pregnant women undergoing hysterectomy. Vascular and myometrial preparations were dissected, mounted in organ baths and isometric tension was recorded. Myometrial strips, but no vascular preparation, developed spontaneous contractile activity. Noradrenaline (NA) and vasopressin (VP) contracted both vessels and myometrium. Prostaglandin F2 alpha (PGF 2 alpha) contracted the myometrial tissue, but had only a minor effect on the vessels. Removal of extracellular calcium almost abolished the myometrial responses to high K+ (124 mM)-solution, PGF 2 alpha, NA and VP. The vascular responses remaining after this treatment were 18% (K+), 34% (NA) and 25% (VP) of control contractions induced by high K+ (124 mM). Nifedipine potently depressed myometrial contractions induced by NA and VP, but was less active against the vascular responses to these agents. In preparations exposed to calcium-free medium, nifedipine (10(-7) M) almost abolished myometrial contractions induced by calcium in the presence of K+ (124 mM), NA or VP. It also effectively depressed vascular responses to calcium in the presence of K+, but was less active if NA and VP were present. It is suggested that PGF2 alpha has almost no contractant effect on intramyometrial arteries, and that the activation process in these vessels is much less dependent on extracellular calcium than that of the myometrium.
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PMID:Differences in contractile activation between human myometrium and intramyometrial arteries. 386 53

1. A constant flow perfusion system using the isolated rat tail has been developed to facilitate the study of resistance vessel behaviour and the action of vasoactive drugs.2. Baseline resistance remains stable for several hours and dose response curves to bolus injections of pressor agents are reproducible when dialysed bovine serum albumen is used in the perfusion medium to maintain osmotic pressure.3. Noradrenaline, adrenaline, serotonin, vasopressin, angiotensin II, high potassium concentrations and sympathetic nerve stimulation constricted the vascular bed.4. Angiotensin I, bradykinin, histamine, acetylcholine and isoprenaline did not alter vascular resistance under baseline conditions.5. Maximal sensitivity to noradrenaline occurred at 32 degrees to 34 degrees C. Below 30 degrees C, resting tone increased and the pressor effect of noradrenaline was prolonged.6. Low concentrations of (+/-)-propranolol in the perfusate enhanced adrenaline and noradrenaline vasoconstriction, high concentration of (+/-)-propranolol had a direct pressor effect and did not affect catecholamine responses.7. The preparation is a simple and relatively inexpensive adjunct to established methods of studying resistance vessel behaviour under varying experimental conditions.
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PMID:Vascular resistance in the perfused isolated rat tail. 431 31

1. The effect of val(5)-angiotensin II amide, noradrenaline and vasopressin, on kidney volume and intrarenal distribution of carbon particles and thioflavine S was examined in the rat.2. Angiotensin produced a dose-dependent shrinkage of the kidney coinciding with the rise in systemic blood pressure. Noradrenaline and vasopressin, however, produced reduction in kidney volume only in much higher doses than were necessary to produce a pressor effect.3. An intravenous infusion of angiotensin sufficient to produce a diuretic response resulted in a striking increase in glomerular content of injected carbon particles, and a marked reduction in filling of the capillary plexuses of the subcortex and outer medulla. The reduction in outer medullary filling was also observed using the thioflavine S technique.4. Noradrenaline infused in amounts sufficient to produce diuresis, aortic constriction above the kidney and vasopressin injection produced no measurable change in carbon particle distribution.5. The reduction in capillary blood flow produced by angiotensin may result in impaired tubular reabsorptive capacity by reducing peritubular removal of reabsorbate, or by reducing oxygen availability. Thus the vasoconstrictor effects of angiotensin may explain its diuretic action.
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PMID:The effect of angiotensin, noradrenaline and vasopressin on blood flow distribution in the rat kidney. 433 28


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