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)

The arginine-8-vasopressin (AVP) responses to osmotic and histamine stimuli were evaluated in 21 patients with central diabetes insipidus (CDI) and compared to those of 10 healthy controls. Plasma AVP was measured by radioimmunoassay. Following the infusion of 2.5% saline, the AVP responses of CDI patients fell into two distinct groups: CDI I gave no response at all, while CDI II responded subnormally. Histamine increased the plasma AVP level significantly in healthy volunteers. Patients with CDI II gave subnormal AVP responses to histamine. The AVP reactions of the patients with CDI I fell into two subgroups: CDI I/A had undetectable plasma AVP, while histamine evoked AVP release in CDI I/B. Histamine trial did not lead to any change in plasma osmolality. The authors conclude that patients with CDI II suffer from a partial CDI, while those with CDI I/A represent a complete form of the disease. The remainder (CDI I/B) presumably have an osmoreceptor failure. Osmotic and non-osmotic stimulation may provide a useful tool in the differential diagnosis of CDI.
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PMID:Plasma arginine-8-vasopressin responses to osmotic or histamine stimulation contribute to the differential diagnosis of central diabetes insipidus. 377 34

The feasibility and validity of endoscopic measurements of gastric mucosal blood flow (GMBF) using 3% H2 gas clearance were investigated in the intact stomach of anesthetized dogs. Platinum electrodes were lengthened and modified to permit passage through the instrument channel of a standard gastroscope. In five anesthetized dogs, antral mucosal blood flow (103.2 +/- 5.3 ml/min/100 g tissue) was significantly higher (P less than 0.05) than that in the corpus (66.9 +/- 7.1 ml/min/100 g tissue). Histamine stimulation selectively increased flow in the corpus to 134.5 +/- 7.5 ml/min/100 g tissue. Comparison of endoscopic GMBF measurements in these five dogs on 2 different days revealed a close correlation (r = 0.87, P less than 0.001). Endoscopic H2 clearance measurements obtained in five awake dogs were not significantly different from those obtained during pentobarbitol anesthesia. In 12 dogs, GMBF determined by endoscopic H2 gas clearance showed a good agreement (r = 0.91, P less than 0.001) with that measured by radioactive microspheres. These two methods also demonstrated comparable changes in GMBF induced by intravenous infusion of histamine and vasopressin. It was concluded that 3% H2 gas clearance can be used to accurately and reproducibly measure GMBF through the endoscope, a unique advantage of this method for potential clinical use.
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PMID:Endoscopic measurements of gastric mucosal blood flow in dogs. 399 Feb 70

1. Hepatic volume was recorded by a plethysmographic technique in cats anaesthetized with pentobarbitone; the hepatic artery and portal vein remained intact. Dose-response curves were obtained for intravenous infusions of adrenaline, noradrenaline, angiotensin, vasopressin and histamine.2. Adrenaline and noradrenaline decreased hepatic blood volume and did not differ significantly in potency. Up to 40% of the hepatic blood volume was expelled by doses within the range secreted by the adrenal medullae.3. Isoprenaline, infused into the hepatic artery, had no significant effect on hepatic blood volume in doses which caused maximal vasodilatation of the hepatic arterial bed. Relaxation of hepatic capacitance vessels mediated by beta-adrenoceptors did not occur.4. Angiotensin infusions in doses previously shown to cause intestinal and splenic vasoconstriction, decreased hepatic blood volume and on a molar or microgramme basis, angiotensin was the most potent of the agents tested. Doses within the probable physiological range of endogenous production decreased hepatic blood volume by up to 20%. The responses were not significantly different when the hepatic nerves were intact or sectioned.5. Vasopressin infusions produced only small decreases in hepatic blood volume. Doses within the range secreted by the posterior pituitary which constrict the intestinal and splenic resistance vessels, did not decrease hepatic blood volume by more than 10%.6. Histamine produced no change in hepatic blood volume in doses which readily produce outflow block in dogs. Either the specific hepatic venous smooth muscle involved in outflow block is absent in the cat or it has no histamine receptors.7. After the rapid change in hepatic blood volume at the onset of the infusion, hepatic volume remained steady for the duration of each infusion. There was no evidence that these agents caused net transsinusoidal fluid movements.
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PMID:Effects of infusions of catecholamines, angiotensin, vasopressin and histamine on hepatic blood volume in the anaesthetized cat. 435 9

1. In dogs anaesthetized with alpha-chloralose, intracerebroventricular (i.c.v.) injection of histamine induced antidiuresis and increase in jugular vein blood antidiuretic hormone (ADH) level but no change in urinary electrolytes. The mechanism of the histamine-induced antidiuretic response was analysed by the use of pharmacological agents.2. Histamine (i.c.v.) in 1-20 mug doses produced a variable effect on urine outflow as well as on the blood ADH concentration; however, higher doses (25-500 mug) of histamine elicited a dose-dependent antidiuretic response with concomitant rise in blood ADH titre.3. Repeated administration of high doses of i.c.v. histamine (400 mug) elicited a diminishing antidiuretic response which was not observable after the fourth dose, thus exhibiting tachyphylaxis. The antidiuretic response to histamine could be restored by central administration of noradrenaline (500 mug).4. Central pretreatment with mepyramine (5 mg) prevented the histamine-induced antidiuresis. Atropine (2 mg i.c.v.) was ineffective in blocking the antidiuretic effect of histamine. A diuretic response to histamine (400 mug i.c.v.) was obtained in phenoxybenzamine (i.c.v.) pretreated animals; this response could be blocked by i.c.v. injection of propranolol. Tetrabenazine pretreatment prevented the antidiuretic response to histamine.5. The results of the study lead us to conclude that histamine releases central catecholamines which activate the central adrenergic mechanism for the release of antidiuretic hormone.
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PMID:Mechanism of histamine-induced antidiuretic response. 472 94

1. Plasma and blood cell volumes were measured simultaneously with [(131)I]albumin and [(32)P]erythrocytes, together with the arterial haematocrits, in acutely splenectomized dogs anaesthetized with sodium barbital. These measurements were made during control runs and after the administration of vasoactive substances.2. With these data and previously derived equations the mean composite radius of all small vessels with a radius < 150 mu, the distribution of the blood volumes between small and large vessels, and other variables could be calculated.3. Adrenaline, CaCl(2) or vasopressin administration caused a reduction of the mean composite radius, a net shift of erythrocytes and plasma out of the small vessel volume, and an expansion of the large vessel volume. Histamine, KCl and MgCl(2) produced opposite effects.4. Adrenaline appeared to cause the release of sequestered erythrocytes into the active circulation.5. The effects of CaCl(2) and KCl persisted for several hours, while those of MgCl(2) did not.6. The effects of vasopressin could be reversed by histamine, those of adrenaline by splenic plasma or KCl, and those of CaCl(2) by MgCl(2).7. It was suggested that the observed vasoactions are essentially the resultants of diverse combinations of direct and indirect actions on the capacitance section of the small vessel volume.
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PMID:Variations in small and large vessel volumes caused by cations, adrenaline and histamine. 603 May 7

The relationship between gastric blood flow and acid secretion has been studied by using a number of secretory stimulants and inhibitors and different techniques that measure gastric blood flow. Although there are conflicting data, there appears to be a consensus regarding the main aspects of this relationship. Agents that stimulate gastric acid secretion such as histamine, gastrin, cholinergic agents, and vagal stimulators also increase gastric blood flow. Other agents such as isoproterenol, epinephrine, and prostaglandins, which at low doses increase gastric blood flow, reduce gastric acid secretion at higher doses. Norepinephrine, vasopressin, and shock reduce gastric blood flow and thereby cause a decrease in secretion. Histamine H2-receptor antagonists reduce stimulated acid secretion and gastric blood flow. Histamine, gastrin, and acetylcholine have been shown to stimulate acid secretion in vitro. Therefore, these observations suggest that although blood flow is not a prerequisite for initiation of stimulated acid secretion, it can become rate-limiting at higher rates of secretion. Although the literature is replete with studies that attempt to characterize the relationship between gastric blood flow and acid secretion, conclusions have varied. Much of the difficulty has arisen because of the differences in technique used to measure gastric blood flow and the differences between anesthetized and unanesthetized animal preparations. Under some specific conditions, the different blood flow techniques give comparable results and this relationship can be defined.
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PMID:Blood flow and gastric secretion. 612 4

Effects of pentagastrin, histamine, PGI2, and vasopressin on gastric mucosal blood flow (GMBF) in innervated stomaches of anesthetized dogs were measured by means of the hydrogen clearance method, using a contact electrode. The results were compared with findings obtained with the aminopyrine (AP) clearance method in Heidenhain pouch preparations. Pentagastrin at 2 and 8 micrograms/kg/hr had no effects on GMBF, as measured by the hydrogen clearance method, but there was a marked increase in GMBF when the AP clearance method was used. Histamine at 40 or 160 micrograms/kg/hr tended to reduce or significantly reduced GMBF when measured with the hydrogen clearance method, but there was a significant increase in GMBF with the AP clearance method. Both PGI2 (3 or 30 micrograms/kg/hr) and vasopressin (0.06 or 0.25 units/kg/hr) reduced GMBF as determined by both methods. These results indicate that the hydrogen clearance method is advantageous for detecting regional GMBF but is disadvantageous when attempting to detect the effects of agents which increase GMBF.
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PMID:Comparative study of hydrogen and aminopyrine clearance methods for determination of gastric mucosal blood flow in dogs. 638 Oct 1

Histamine levels were determined in whole hypothalamus and specific hypothalamic nuclei of male 9-week-old homozygous Brattleboro rats lacking vasopressin and presenting the syndrome of diabetes insipidus (DI rats). These levels were compared to those in heterozygous Brattleboro rats with a partial deficit in vasopressin (HZ rats) and those in Long Evans control rats (LE rats). In whole hypothalamus, histamine levels in DI rats were higher than those found in HZ and LE rats. DI rats showed histamine levels higher than those present in LE rats in the nuclei supraopticus, paraventricularis and suprachiasmatis and in the area retrochiasmatica. Vasopressin replacement produced a selective decrease in histamine levels of DI rats, restricted to the area retrochiasmatica and nuclei supraopticus and paraventricularis. In contrast, vasopressin increased histamine levels in the area retrochiasmatica and eminentia mediana of HZ rats. In other areas normally rich in vasopressin such as the nucleus arcuatus and the eminentia mediana, the histamine content was not different among LE, HZ or DI rats. Our results suggest a physiological interaction between vasopressin and histamine systems in specific hypothalamic areas of the rat and support the hypothesis of a role of brain histamine on the central control of water balance.
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PMID:High histamine levels in specific hypothalamic nuclei of Brattleboro rats lacking vasopressin. 662 8

The mechanism for the pressor response to intracerebroventricularly (i.c.v.) administered histamine was studied. Histamine (HA), when injected intracerebroventricularly in rats, produced a dose-dependent increase in mean arterial pressure (MAP) which was subject to tachyphylaxis. Spinal transection at C-7 in the anesthetized rat did not attenuate the rise in blood pressure. The possibility that the release of 8-arginine vasopressin was responsible for the rise in blood pressure was explored. By pretreating conscious freely-moving rats with a specific antagonist to the vasopressor action of vasopressin viz., [1-beta-mercapto-beta, beta-cyclopentamethyleneproprionic acid), 2-(O-methyl) tyrosine] arginine-vasopressin, there was a statistically-significant attenuation of the pressor response to intracerebroventricularly administered histamine. The antagonist however, did not totally abolish the pressor response, regardless of the dose employed. Concomitant administration of hexamethonium and the vasopressin antagonist did not further attenuate the response. Previous adrenal demedullation did not diminish the response to intracerebroventricularly administered histamine, nor was there any evidence for release of angiotensin II since pretreatment with saralasin did not attenuate the cardiovascular response. These findings suggest that vasopressin along with other as yet undefined substances, are released from the central nervous system to produce the increase in blood pressure after intracerebroventricularly administered histamine.
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PMID:The effect of a vasopressin antagonist on the pressor response to histamine administered centrally. 668 61

Histamine H1-agonists 2-pyridylethylamine (2-PEA) and 2-methylhistamine and H2-agonists 4-methylhistamine, dimaprit and impromidine were given i.c.v. to conscious goats and the release of arginine vasopressin (AVP) was measured. 2-PEA at very low doses (9 and 27 mumoles/animal, equivalent to H1-activity of about 0.5 and 1.5 mumoles histamine, resp.) significantly increased plasma AVP. The H2-agonists did not cause consistent changes in AVP even if their relative doses were higher. It is concluded that the vasopressin releasing effect of histamine is due to H1-receptor activation.
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PMID:Plasma vasopressin levels after I.C.V. infusion of histamine agonists in the conscious goat. 673 Nov 86


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