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 effect of [1-(beta-mercapto-beta,beta- cyclopentamethylene -propionic acid)2-0- ethyltyrosine ,4-valine] arginine vasopressin on the water metabolism was studied in rat. The compound was found to be able to block the antidiuretic action of both exogenous and endogenous vasopressin. A rat model of the Schwartz-Bartter syndrome was created by the administration of a high dose of a posterior pituitary preparation (Pitressin tannate ) together with a forced water intake. The antagonist prevented water retention and averted the enhanced natriuresis and hyponatraemia, and cerebral oedema did not develop. The observations suggest that this vasopressin antagonist might be of use in the future as an effective drug against the Schwartz-Bartter syndrome.
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PMID:Effect of the vasopressin antagonist d(CH2)5 Tyr(Et)VAVP on diuresis in rat. 673 24

The distribution of vasotocin and isotocin in the brain of the rainbow trout Salmo gairdneri was investigated by the unlabeled antibody enzyme method, by using purified antisera against arginine vasotocin and isotocin. In the preoptic nucleus no clear differences were observed in the distribution of vasotocin- and isotocin-containing cells. Vasotocin and isotocin innervation was found in most brain regions, though in general isotocin fibers were much more abundant. The area dorsalis pars medialis of the telencephalon, the saccus dorsalis, and the basal part of the nucleus recessus posterioris were found to be innervated by vasotocin and scarcely by isotocin fibers. In the nucleus habenularis, the nucleus recessus lobus lateralis, the nucleus preglomerulosus pars medialis, and the tectum mesencephali isotocin fibers prevailed. These findings in the trout brain are compared with the vasopressin and oxytocin innervation of the rat brain.
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PMID:The distribution of vasotocin and isotocin in the brain of the rainbow trout. 676 94

The effects of fluid intake on basal and vasopressin-responsive urinary PGE excretion (UPGEV) were examined in conscious rats under conditions of 1) ad libitum water intake, 2) water deprivation, and 3) water diuresis induced by ad libitum intake of 5% dextrose in water. UPGEV fell progressively during 40 h of water deprivation. Water diuresis after water deprivation increased UPGEV transiently (8 h). Vasopressin (Pitressin tannate in oil, 5 U/kg subcutaneously) increased UPGEV and decreased urine volume (V) in rats on ad libitum water intake but did not alter UPGEV during water deprivation. Indomethacin suppressed UPGEV (70-90%), increased basal urine osmolality (Uosmol), and potentiated the antidiuretic response to Pitressin in rats on ad libitum water intake. Indomethacin accelerated by 8 h the onset of maximal antidiuresis in water-deprived rats but did not significantly alter water balance. During water diuresis, UPGEV declined in the first 8 h after Pitressin. Thereafter, UPGEV increased markedly, concurrent with early vasopressin escape. Indomethacin or meclofenamate inhibited the rise in UPGEV, the decline in Uosmol, and the increase in V of the escape phase. Indomethacin or meclofenamate also impaired the excretion of an acute water load (5% body wt) given during escape. The spontaneous decline in UPGEV during hydropenia may serve to maximize physiologic antidiuresis. Conversely, the marked increase in UPGEV induced by administration of vasopressin during water diuresis may serve to suppress the antidiuretic response and thus play a role in the mediation of escape from physiologically inappropriate antidiuresis.
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PMID:Effects of fluid intake on basal and vasopressin-responsive urinary prostaglandin E. 686 38

Decreasing hematocrit values were observed in chick embryos, from Day 17 to 1 day posthatching. Arginine vasotocin (AVT) and mesotocin (MT) were determined radioimmunologically in serum, neural lobe, and hypothalamic tissue. Serum levels of AVT and MT were significantly increased on Day 18 of incubation compared to Day 17. Thereafter AVT levels decreased, reaching at hatching levels even below Day 17. Serum MT remained elevated on Day 19, but decreased thereafter to the concentration values of Day 17. The amount of AVT in the preoptic hypothalamus and infundibulum was maximal on Day 19, whereas in the neural lobe the maximum was attained on Day 20. The MT content of the infundibulum and neural lobe reached a maximum plateau on Day 18. These results suggest that a stimulation of the hypothalamo-neurohypophyseal axis in the chick embryo occurs at the end of incubation. A possible causal relation with the observed decreasing hematocrit values is discussed.
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PMID:The presence of vasotocin and mesotocin in serum and the hypothalamo-neurohypophyseal axis of chick embryos before hatching and in posthatch chicks. 688 49

Antidiuretic hormone (ADH) (200 microunits/ml Pitressin or synthetic arginine vasopressin) causes a transitory increase followed by a sustained decrease in the potential difference (PD) and in the net fluxes of sodium and chloride across rabbit cortical collecting tubules perfused in vitro. The inhibitory action of vasopressin is reversible; removal of the hormone from the bath promotes recovery in the PD and in the transport of sodium and chloride to the level of the controls. After 70 min of incubation with ADH, 10(-5) M meclofenamate, an inhibitor of the synthesis of prostaglandins, was added to the bath of some tubules. Despite the presence of ADH, the PD and ionic fluxes increased to control levels. The introduction of exogenous prostaglandin E2 (10(-5) M PGE2) to the bathing medium containing ADH and meclofenamate mimicked the inhibitory action of ADH, decreasing the PD and the reabsorption of sodium and chloride. Pretreatment of collecting tubules with meclofenamate prevented the inhibitory effect of ADH. These findings show that vasopressin exerts a prolonged inhibitory action on PD and on net reabsorption of Na and Cl and that this action may be exerted through stimulating the biosynthesis of prostaglandin E2 by the cortical collecting tubule.
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PMID:ADH-PGE2 interactions in cortical collecting tubule. I. Depression of sodium transport. 694 96

In the absence of ADH, microperfused cortical collecting tubules of rabbits reabsorb calcium and phosphorus. Antidiuretic hormone (ADH) (200 microunits/ml Pitressin or synthetic arginine vasopressin) inhibits the reabsorption and may promote the secretion of calcium and phosphorus. At 5 min after incubation with ADH, there was a transitory increase in the potential difference and the reabsorption of sodium. The fluxes of calcium and phosphorus, however, showed no significant change from the control values. At 30-50 min after treatment with ADH, the reabsorption of calcium and phosphorus was inhibited and in some tubules calcium and phosphorus were secreted. The removal of vasopressin from the bath or the addition of 10(-5) M meclofenamate in vitro prevented ADH from inhibiting the reabsorption of calcium and phosphorus. Treatment of tubules with 10(-5) M prostaglandin E2 (PGE2) subsequent to incubation in a medium containing ADH and meclofenamate inhibited the reabsorption or even promoted the secretin of calcium and phosphorus, as did the prolonged incubation with ADH alone. We conclude that cortical collecting tubules reabsorb calcium and phosphorus in the absence of vasopressin and that ADH inhibits calcium and phosphorus reabsorption. Endogenous synthesis of PGE2 may mediate the inhibitory action of ADH, since meclofenamate (an inhibitor of the synthesis of prostaglandins) opposes and exogenous PGE2 mimics ADH.
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PMID:ADH-PGE2 interactions in cortical collecting tubule. II. inhibition of Ca and P reabsorption. 694 97

We reviewed the courses of 40 patients with variceal bleeding treated with a standardized protocol, including intravenous (IV) vasopressin (Pitressin) and transhepatic embolization. Twelve of the 32 patients with acute episodes of massive variceal bleeding responded to the administration of IV vasopressin alone. Of the 20 patients who did not respond to vasopressin therapy, emergency transhepatic portography with embolization produced cessation of bleeding in ten (50%). The remaining ten patients who failed to respond to either IV vasopressin therapy or transhepatic embolization died, regardless of whether they were treated with aggressive medical therapy or emergency portosystemic shunt. Transhepatic embolization in both the emergent and elective situation demonstrated a thrombotic complication rate of 20%, which limited or precluded eventual therapy with elective portosystemic shunt. Because of this relatively high incidence of occult portal thromboses after transhepatic embolization, transhepatic portography should be obtained routinely prior to elective portosystemic shunts in those patients who have a history of transhepatic embolization.
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PMID:Management of variceal hemorrhage: results of a standardized protocol using vasopressin and transhepatic embolization. 696 50

The management of patients with gastrointestinal (GI) bleeding depends on accurate localization of the site of hemorrhage. Endoscopy and arteriography, although successful in achieving this goal in the majority of patients, are invasive and have other shortcomings. The introduction of the 99mTc-sulfur colloid technique has greatly simplified the evaluation and management of these patients. This test is useful in detecting and localizing the bleeding site in the lower GI tract. Scintigraphy is now used as the initial study of choice in patients with rectal bleeding. Advances made in angiography and nuclear medicine techniques also have resulted in improved management of patients. Conservative approaches succeed in controlling hemorrhage in most patients. Vasopressin is the most widely tested agent and has been adopted by many as the preferred preparation for this purpose. Before the introduction of the 99mTc-sulfur colloid technique, angiography was used to monitor the effectiveness of this drug, whether administered intravenously or intraarterially. With the use of scintigraphy and intravenous administration of vasopressin, these patients now can be managed noninvasively. Only when the intravenous Pitressin infusion fails to stop hemorrhage, is the intraarterial approach considered. Surgery is used as a last resort when these measures fail to stop the bleeding.
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PMID:Studies of GI bleeding with scintigraphy and the influence of vasopressin. 697 2

In two-kidney one-clip hypertensive rats we evaluated the effect of water restriction on the development and maintenance of severe hypertension (systemic blood pressure 200-230 mmHg). After application of renal arterial clips in rats allowed access to water for 1 or 2 h daily, BP stabilized at 180-190 mmHg. No increase in water intake occurred and plasma renin activity(PRA) (measured before the drinking period) was significantly below the levels observed in ad libitum-drinking hypertensive rats. In rats administered 4 ml water/100 g body weight twice daily by gavage, development of hypertension was more clearly suppressed. Blood pressure increased slowly and reached levels of only 150-170 mmHg. Furthermore, PRA was significantly lower in this group compared with ad libitum-drinking hypertensive animals. In rats with established (4-5 wk) renal hypertension, restriction of water intake to 1 or 2 h daily resulted in a rapid decrease in BP of about 30 mmHg. Daily administration of Pitressin tannate to hypertensive rats allowed free access to water induced a similar decrease in BP as well as suppression of PRA. These results indicate that the hypotensive effect of water restriction in the two-kidney one-clip hypertensive rat model may be mediated, at least in part, through elevated circulating levels of vasopressin that subsequently inhibit renin release.
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PMID:Hypotensive effect of water restriction in the two-kidney one-clip hypertensive rat. 703 85

Vasopressin produced analgesia in mice as estimated by using abdominal constriction tests (ED50 8.5 micrograms/kg i.v.) or hot plate method (ED50 63 micrograms/kg i.v.). However, vasopressin (10 micrograms/kg i.v.) produced no depression of locomotor activity in mice. Vasotocin had slight analgesic action; oxytocin or norepinephrine had none and there was no direct correlation between pressor response and analgesia. The analgesic action was nonopiate in nature as it was uninfluenced by the narcotic antagonist naltrexone at 5 to 15 mg/kg, but it was reserved by a vasopressin antagonist. Intraventricular administration of vasopressin (1-10 micrograms/kg) to mice produced no significant analgesia, suggesting a primarily peripheral locus of analgesic action. Vasopressin may play a role as an endogeneous pain regulating substance.
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PMID:Characterization of vasopressin analgesia. 705 94


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