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)

1. Vaginal dilatation for 30 seconds caused a rapid and brief increase in intramammary pressure which was equivalent to that evoked by 160 muU of oxytocin (Syntocinon) injected intravenously. 2. The rise in mammary pressure induced by the stimulation of the central end of a severed vagus nerve for 30 seconds (5 V, 0,5 ms, 50 HZ) was similar to the response obtained with an intravenous injection of 360 muU of oxytocin. 3. The vago-pituitary reflex leads to the liberation of large amounts of antidiuretic hormone which does not interfere with the effect of oxytocin on the mammary gland, since dexamethasone phosphate prevented the vasopressor effect without significantly affecting the increase in intramammary pressure.
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PMID:[Level of oxytocin release induced by vaginal dilatation (Ferguson reflex) and vagal stimulation (vago-pituitary reflex) in lactating rats (author's transl)]. 120 94

The influence of a i.v. injection of 2 I.U. of synthetic oxytocin (Oxy, Syntocinon) on plasma cortisol has been tested in 6 normal volunteers (age 22 to 33) and compared to a similar saline injection in a blind, cross-over design. Before injection basal cortisol is similar in Oxy (12.1 +/- 2.3 micrograms/100 ml M +/- Se) and saline (11.7 +/- 3.5) groups; in the Oxy group a significant (2 p less than 0.01) decrease of cortisol was noticed from the 45th min until the end of the test (120 min): the last mean level being 5.2 +/- 0.9 in the Oxy group compared to 12.9 +/- 1.8 in the saline group (2 p less than 0.005). Although the mechanism of action of Oxy on cortisol plasma levels remains to be investigated our results are in agreement with a proper action of Oxy and vasopressin at the level of the corticotroph cells or with a proper action of Oxy or of one of its metabolite (Pro-Leu-Gly-NH2 for example) on proopiomelanocorticotropic function.
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PMID:[Intravenous injection of synthetic oxytocin induces a decrease of cortisol plasma level in normal man]. 645 79

In order to test a possible stimulatory effect of oxytocin and lysine-vasopressin on prolactin (PRL) release six female volunteers received either saline or 1 IU oxytocin (Syntocinon) i.v.. Blood sampling was performed at intervals over 90 minutes. Nine puerperae were treated with oral oxytocin (Sandopart) 50 IU t.i.d. for seven days. Nine other untreated postpartum women served as controls. Blood was collected before delivery and on subsequent postpartum days, and the milk volumes produced were estimated by increases in the babies' weight. In addition, seven volunteers received 5 or IU lysine-vasopressin (Vasopressin) i.m. Blood was withdrawn at regular intervals for 180 minutes, the urine volumes excreted in 30-minute intervals were measured and the clearance of free water calculated. Oxytocin failed to modify basal plasma PRL in the acute trial and in the post-partum women, and milk amounts produced were not influenced by treatment. Vasopressin did not change the PRL plasma profile despite a significant (p less than 0.05) reduction in the excretion of free water. Results indicate that neuropeptides are not implicated in the control of PRL release.
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PMID:Failure of oxytocin and lysine-vasopressin to stimulate prolactin release in humans. 718 25

Valyl(3)-oxytocin has similar circulatory effects in man to those of Syntocinon (synthetic oxytocin). On intravenous administration, it caused a rise in limb blood flow and in pulse rate and a fall in blood pressure. It had a direct vasodilator effect on limb blood vessels. Valyl(3)-oxytocin was 1.5 to 2 times more potent than Syntocinon in terms of its circulatory effect in man. The circulatory effects of valyl(3)-oxytocin were less readily antagonized by vasopressin than are those of Syntocinon.
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PMID:Comparison of effects of valyl(3)-oxytocin and syntocinon on the cardiovascular system of man. 1440 99

Synthetic oxytocin (Syntocinon) can be shown to reduce or abolish ST-T changes induced experimentally by hypoxaemia alone, by hypoxaemia and ergometrine, by vasopressin, and by a new procedure involving injection of small doses of picrotoxin into the lateral cerebral ventricle. Ventricular fibrillation induced by picrotoxin can also be reversed by oxytocin. These effects suggest a probable metabolic action of oxytocin against cardiac anoxic changes, and its possible therapeutic usefulness as an antagonist of myocardial ischaemia. It is speculated that this might be a physiological action of the hormone.
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PMID:Synthetic oxytocin as an antagonist of experimental cardiac anoxic changes in rabbits. 1447 82