Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The contractile responses of helically cut vascular strips of chickens to vasoactive agents were studied.2. Large pulmonary arteries were contracted by neurohypophysial peptides, but not by angiotensin, acetylcholine, histamine, 5-hydroxytryptamine, bradykinin or eledoisin. The activity of oxytocin was greater than that of arginine vasopressin.3. Vasodilator effects of oxytocin upon small (200-500 mu diameter) mesenteric and muscular arteries were demonstrable, but inconsistent.4. Magnesium potentiated in a parallel fashion the vasoconstrictor effects of oxytocin and of arginine vasopressin.5. Deamino-oxytocin was potentiated by magnesium. This finding suggests a difference between the peptide-protein interactions of tissue receptors and those of neurophysin.
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PMID:Neurohypophysial peptide interaction with magnesium in avian vascular smooth muscle. 429 87

1. The epigastric adipose tissue of rabbits has been prepared so that the effects of close arterial injections and infusions on blood flow and release of free fatty acids (FFA) can be studied. The effects of pharmacologically active agents and hormone preparations have been investigated.2. Release of FFA was stimulated by synthetic adrenocorticotrophic hormone (ACTH), alpha and beta melanophore stimulating hormone (MSH), porcine growth hormone, glucagon, thyrotropic hormone (TSH) and luteotropic hormone (LTH). Single injections of fat-mobilizing agents produce a sustained rise in the release of FFA.3. Although pitressin caused release of FFA, synthetic vasopressin and oxytocin failed to do so. The FFA releasing activity of pitressin has therefore been attributed to a contaminant.4. Catecholamines were found not to stimulate release of FFA from this fat depot, but were found to increase plasma FFA when infused intravenously.5. Injections of acetylcholine, histamine, bradykinin, 5-hydroxytryptamine, synthetic arginine vasopressin, and lysine vasopressin, oxytocin, angiotensin and FSH did not stimulate release of FFA although marked effects on blood flow were produced.6. Injections of prostaglandin E(1) gave sustained increases in blood flow, and inhibited FFA release when stimulated by growth hormone.7. The mobilization of FFA is sometimes associated with an increased rate of blood flow.
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PMID:The mobilization of free fatty acids from rabbit adipose tissue in situ. 430 78

1. Metals potentiate the contractile effects of S-S polypeptides in depolarized rat uterus. Their order of potency is Co(++)>/=Co(+++)>/=Mn(++)>/=Ni(++)>/= Mn(+++)>Zn(++)>/=Mg(++)>Fe(++)>Fe(+++)>/= Ca(++)>Be(++)=Sr(++)=Ba(++)=Cu(++)=O.2. S-S polypeptides with relatively weak oxytocic activity such as lys-vasopressin, arg-vasopressin and orn-vasopressin are strongly potentiated by metals while highly active polypeptides such as oxytocin are weakly potentiated.3. Potentiation by metals was specific for S-S polypeptides; other polypeptides (bradykinin, hypertensin) as well as acetylcholine and isoprenaline were unaffected.4. Potentiation by metals occurs rapidly and is fully reversible. In all cases some activity was retained by S-S polypeptides even in the complete absence of metals.5. A scheme which could account for the observed effects has been formulated. This assumes the formation of a ternary complex between receptor, metal and polypeptide leading to improved alignment between polypeptide and receptor.6. Analogies are discussed between metal enzymes and the S-S polypeptide receptor for which the term metal receptor is proposed.
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PMID:The effect of metals on the S-S polypeptide receptor in depolarized rat uterus. 430 88

1. A synthetic oxytocin analogue, [1-N-carbamoyl-hemicystine-2-O-methyltyrosine]-oxytocin (carbamoyl-methyloxytocin), has been tested as an antagonist to the actions of oxytocin and vasopressin on the uterus, the mammary gland and blood pressure.2. The analogue inhibited the response of the isolated rat uterus to both oxytocin and vasopressin without itself stimulating the uterus to contract. The responses to equipotent doses of oxytocin and vasopressin were inhibited equally. There was little or no inhibition of the response to bradykinin. carbachol, angiotensin or 5-hydroxytryptamine with doses of the analogue up to 160 times that required to inhibit the response to oxytocin by 50%. The analogue caused a parallel displacement of the log dose-response curve for oxytocin; the pA(2) value (2 min contact) varied from 6.4 to 7.1 according to the ionic composition of the solution in the organ bath.3. The analogue inhibited the response of the rat uterus in situ to oxytocin but not to angiotensin or 5-hydroxytryptamine. It did not stimulate the uterus.4. When, in certain experimental conditions, spontaneous activity occurred in the isolated uterus or the uterus in situ, this activity was unaffected by the analogue but the increase in amplitude and frequency of contractions caused by oxytocin was inhibited. The regular rhythm of contractions induced in the quiescent uterus by the intravenous infusion of oxytocin was interrupted by intravenous injections of the analogue.5. The response of the isolated strip of rat mammary gland to the analogue depended on whether or not magnesium was present in the bath solution. In the presence of this ion, the analogue generally caused an increase in tension; in its absence, it acted as a pure antagonist. As on the isolated uterus, oxytocin and vasopressin were equally inhibited, and the analogue caused a parallel displacement of the log dose-response curve for oxytocin. With 0.9 mM Ca and 1.0 mM Mg, the mean pA(2) value (2 min contact) was 6.28 +/- 0.08 (S.E.)6. In the lactating rat, the analogue inhibited the milk-ejection response to oxytocin and vasopressin but not that to acetylcholine, bradykinin or 5-hydroxytryptamine. A milk-ejection response to the analogue itself was seen occasionally with retrograde arterial but not with intravenous injections.7. The analogue inhibited the avian depressor response to oxytocin and the rat pressor response to vasopressin.8. On all assay preparations, the degree of inhibition caused by the analogue was dependent on the dose, and the inhibition could be surmounted by increasing the dose of agonist. Recovery usually occurred within 15 min. These features, together with the parallel displacement of the dose-response curve for oxytocin on the isolated uterus and mammary strip, and the equal inhibition of the responses to oxytocin and vasopressin, suggest that carbamoyl-methyl-oxytocin acts as a specific competitive inhibitor of the neurohypophysial hormones.9. The structure-activity relationships of analogues of oxytocin having substituents in the terminal amino and phenolic hydroxyl groups, and some practical applications of the carbamoyl-methyl analogue, are discussed.
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PMID:Some pharmacological properties of a synthetic oxytocin analogue [1-N-carbamoyl-hemicystine-2-O-methyltyrosine]-oxytocin (carbamoyl-methyloxytocin), an antagonist to the neurohypophysial hormones. 432 60

1. Recently it has been shown that injection of angiotensin II into the anterior diencephalon causes the rat to drink water. In the present experiments the dipsogenic action of a number of other substances including substances related to angiotensin was tested.2. Injection of 0.001 Goldblatt u. renin into the angiotensin-sensitive region causes the water-replete rat to drink. Drinking is slower in onset and continues for longer than after injection of angiotensin II.3. Synthetic tetradecapeptide renin substrate and angiotensin I were as effective as angiotensin II at causing water-replete rats to drink.4. beta-aspartic acid(1)-valine(5)-angiotensin II was also fully effective; but the D-arginine substituted octapeptide was much less effective.5. The (2-8) heptapeptide retained about 50% of the dipsogenic activity of the octapeptide, whereas the absence of phenylalanine at the other end of the peptide chain in the (1-7) heptapeptide results in an inactive compound.6. The (3-8) hexapeptide and the (4-8) pentapeptide, both of which have phenylalanine at the end of the chain, and the (1-4) and (5-8) tetrapeptide fragments of angiotensin II showed only a slight action on intake of water.7. Kallikrein, bradykinin, adenosine-3'5-cyclic phosphate, vasopressin and oxytocin caused no drinking when injected into the angiotensin-sensitive region.8. It is concluded that the requirements for the dipsogenic activity of angiotensin are the same as those for its other biological actions with the qualification that the precursor peptides are also active, presumably because they give rise to angiotensin II locally.
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PMID:The effect on drinking of peptide precursors and of shorter chain peptide fragments of angiotensin II injected into the rat's diencephalon. 432 62

1 A sensitive method of assaying oxytocin using the superfused mouse mammary gland is described. The method is shown to be reliable, accurate and precise. Assays are performed automatically and the preparation is stable for at least 18 hours.2 The preparation is relatively insensitive to bradykinin, histamine, 5-hydroxytryptamine, angiotensin, prostaglandin F(2alpha), adrenaline and noradrenaline. The contractions produced by acetylcholine can be abolished by atropine without the sensitivity to oxytocin being affected.3 Vasopressin has a variable activity on the preparation; its potency can be as high as one-fifth that of oxytocin.4 It is concluded that this method compares favourably with other published methods.
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PMID:Bioassay of oxytocin on the superfused mammary gland of the mouse, using an automatic apparatus. 436 53

1. A search was made for an assay tissue with selective sensitivity to vasopressin. Of those smooth muscle preparations tested, the longitudinal muscle of the isolated rectum of the rabbit was the most satisfactory.2. The rabbit isolated rectum, bathed in Krebs solution, was contracted by acetylcholine, angiotensin II amide, bradykinin and 5-hydroxytryptamine. It was relaxed by vasopressin, oxytocin and the catecholamines.3. Vasopressin was active in concentrations of 4-100 muu./ml (0.01-0.25 ng/ml) and was 20-30 times more active than oxytocin. Bretylium had no effect on the relaxant action of vasopressin; nor did concentrations of alpha- and beta-adrenoceptor blocking agents sufficient to abolish the actions of catecholamines. Lignocaine reduced the sensitivity of the rabbit rectum to both vasopressin and oxytocin without altering the actions of adrenaline. High concentrations of either vasopressin or oxytocin desensitized the rabbit rectum to the actions of both hormones, without affecting the actions of adrenaline. It was concluded that vasopressin and oxytocin act on a common population of receptors different from those for catecholamines.4. Phentolamine, unlike other alpha-adrenoceptor antagonists, reduced the relaxant action of vasopressin on the rectum.5. When superfused with blood from an anaesthetized dog, the rabbit rectum maintained a higher tone than in Krebs solution; it retained its sensitivity to vasopressin. Pronethalol, administered intraluminally, reduced spontaneous movement and abolished the actions of low concentrations of catecholamines, thereby increasing the specificity of the assay. No other substance tested relaxed the rectum in concentrations likely to be found in blood.6. Vasopressin was stable in dog's blood; it survived passage through the pulmonary vascular bed; it had a half-life in the circulation of about 1 min.7. The half-life of vasopressin in the circulation may depend upon the duration of the infusion.
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PMID:A sensitive and specific assay for vasopressin in the circulating blood. 439 59

1. When goats were milked each hour after being given a dose of synthetic oxytocin within the range thought to be released by the pituitary, there was a progressive rise in milk yield becoming statistically significant by 5 hr. The effect was reduced if the milk was not removed from the gland each hour.2. Milking transplanted glands each hour without injecting oxytocin also increased milk yield. The yield of the unmilked glands on the same animals was not affected. Massaging the transplanted glands had no effect on the milk yield.3. Oxytocin treatment and, to a lesser extent, frequent milking without oxytocin, altered milk composition. [Na], [Cl] and [non-casein protein] increased; [K] and [lactose] decreased.4. Oxytocin infusions permitted the leakage of [(14)C]lactose from milk to plasma and [(14)C]sucrose from plasma to milk.5. In some goats very small doses of oxytocin caused changes in milk composition and in one such animal these changes were mimicked by the close arterial infusion of bradykinin.6. Reasons are given for believing that the changes in composition are incidental to the main action of oxytocin in expelling milk and could be caused by a small number of leaks between the tight junctions connecting secretory cells.7. The increase in the rate of milk secretion following milk removal is probably of greater physiological significance than the small changes in milk composition and supports Levy's idea of a local negative feed-back via a chemical component of milk.
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PMID:The effects of oxytocin and milk removal on milk secretion in the goat. 510 50

1. Pressure changes in the submaxillary and parotid ducts of dogs, induced by nerve stimulation or intravenous injection of drugs, were studied.2. Pressure rises could be elicited by parasympathetic stimulation and by acetylcholine and methacholine, even when no secretion was evoked. These effects were abolished by atropine.3. Similarly, sympathetic stimulation, adrenaline, noradrenaline and phenylephrine raised the pressure in both glands, also in the absence of secretion. Dihydroergotamine abolished these effects. Isoprenaline increased the pressure in the submaxillary duct, but only when it caused secretion. This effect was abolished by propranolol. In the parotid gland isoprenaline caused neither secretion nor pressure rise. It is concluded that the myoepithelial cells of the two glands are supplied with alpha-adrenoceptors.4. Doses of histamine, bradykinin, kallidin and physalaemin which caused no salivary secretion raised the duct pressure even when dihydroergotamine, propranolol and atropine had been given.5. Angiotensin and 5-hydroxytryptamine increased the pressure only in some experiments. Oxytocin caused very little or no pressure rise. Vasopressin had no effect of its own but reduced the pressure raising effects of nerve stimulation or drugs.
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PMID:The pharmacology of salivary myoepithelial cells in dogs. 534 69

1. An oxytocic substance has been isolated from ox hypothalamus by successive gel filtration on Sephadex G-25 and Sephadex G-50, and its pharmacology has been examined on three smooth muscle preparations.2. The substance has the same order of potency on rat uterus, guinea-pig ileum, and hen rectal caecum.3. The action of the substance on rat uterus was not abolished by thioglycollate.4. Atropine (1.0 mug/ml.), phenoxybenzamine (0.1 mug/ml.) and mepyramine (1.0 mug/ml.) did not block the smooth muscle action of the substance.5. Drug action, relative potency, and log dose-response relationships distinguish the substance from 5-hydroxytryptamine, acetylcholine, oxytocin, vasopressin, angiotensin amide, bradykinin, and purified preparations of substance P.
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PMID:The pharmacology of a new oxytocic principle from ox hypothalamus. 581 85


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