UNIPROT:P01185 - FACTA Search

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

Oxytocin (OT) and vasopressin (VP) were measured by radioimmunoassay in hypophysial portal and peripheral blood from male Wistar rats and heterozygous and homozygous Brattleboro rats anaesthetized with urethane. In Wistar rats the concentrations of OT and VP were about 50 times greater than the concentrations in peripheral blood, whether or not the pituitary gland was left in situ during collection, and also considerably greater than the reported concentrations of the peptides in the cerebrospinal fluid. The release of both peptides was increased significantly by a lesion of the supraoptico-hypophysial tract that led to diabetes insipidus, but which left intact the external layer of the median eminence (ME). Concentrations of VP were undetectable in plasma from homozygous Brattleboro rats, but the portal plasma concentrations of VP in heterozygous Brattleboro rats were not significantly lower than in Wistar rats. The concentrations of OT in portal plasma from both types of Brattleboro rat were significantly higher than in Wistar rats. The output of VP and OT into hypophysial portal blood of Wistar rats was not significantly affected by electrical stimulation of the suprachiasmatic, supraoptic or paraventricular nuclei or the ME using two types of stimuli, one of which produced an increase in peripheral plasma concentrations of VP and OT in intact rats and a significant increase in the release of LH-releasing hormone into hypophysial portal blood. The output of VP and OT into portal blood was also not significantly affected by either adrenalectomy with or without injection of dexamethasone or the injection of either the 5-hydroxytryptamine (5-HT) synthesis blocker, parachlorophenylalanine, or the 5-HT uptake blockers, alaproclate or zimelidine. These results show that large amounts of OT as well as VP are released into hypophysial portal blood from fibres of the hypothalamo-neurohypophysial system that terminate in the external layer of the ME. Although distinct from the fibres that terminate in the pars nervosa (PN), the findings in Brattleboro rats show that the VP fibres of the ME system originate in neurones with a genomic mechanism for VP synthesis similar to that of the VP neurones that project to the PN. The lack of effect of adrenalectomy and the administration of 5-HT synthesis and uptake blockers must be interpreted with caution since the results obtained with electrical stimulation suggest that when the pituitary stalk is cut the release of OT and VP into portal blood approaches a maximum and may therefore be difficult to alter by experimental manipulation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Oxytocin and vasopressin in rat hypophysial portal blood: experimental studies in normal and Brattleboro rats. 396 10

Intrinsic vascular responsiveness was examined in isolated, helically cut strips of cystic artery from 32 normotensive women. Contractions were elicited by vasopressin, norepinephrine, 5-hydroxytryptamine and transmural electrical stimulation. Of the 32 subjects, 17 had a family history of hypertension in a first-degree relative (parent, sibling, or adult offspring) and 15 had no family history of hypertension. The ages and mean arterial blood pressures of the two groups were not different: 39 +/- 12 versus 35 +/- 11 years (mean +/- SD; p = 0.263) and 87 +/- 4 versus 85 +/- 5 mm Hg (p = 0.214) respectively. The vasopressin dose-response curve was significantly shifted to the left for arteries of those subjects with a family history of hypertension compared with that for arteries of subjects with no family history (e.g., response--percent of norepinephrine maximum--to 100 mU/ml = 31 +/- 23 versus 12 +/- 16; p = 0.014). All other responses were not significantly different, although in general the arteries of those subjects with a family history tended to have greater responses to all stimuli except norepinephrine. Arteries from the two groups did not differ with respect to physical dimensions (e.g., cross-sectional area), passive mechanical properties, or maximal responses to norepinephrine. The data indicate that altered intrinsic vascular responsiveness is linked to a family history of hypertension in normotensive subjects and thus could play a role in the familial aggregation of elevated blood pressure.
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PMID:In vitro arterial responses to vasopressin in subjects with a family history of hypertension. 398 67

Pig isolated renal arteries contract in response to addition of noradrenaline, 5-hydroxytryptamine, histamine, angiotensin II, vasopressin and carbachol, whereas cholecystokinin, adenosine, and inosine produce relaxation. Transmural stimulation of the tissue causes contraction of circular muscle in the arterial wall which produces apparent elongation of the vessel. The effects of transmural stimulation are partially blocked by prazosin and potentiated by propranolol, indicating that noradrenaline acts through both alpha- and beta-adrenoceptors. Guanethidine (10(-5) M) reduces the size of responses to transmural stimulation in the presence of both prazosin (10(-6) M) and propranolol (10(-7) M). Both saralasin (10(-7) M), and desensitization of angiotensin II receptors by prolonged contact with the peptide, produced a reduction in response to transmural stimulation, indicating that angiotensin II may be involved in neurotransmission. This effect was blocked by tetrodotoxin. Transmural stimulation produces relaxation of renal arteries in the presence of maximal doses of saralasin, prazosin, and propranolol, suggesting that a third unidentified substance is also released from autonomic nerves.
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PMID:Responses of the pig isolated renal artery to transmural electrical stimulation and drugs. 400 89

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. 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. 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 The cat anococcygeus muscle is shown to possess a dual innervation similar to the rat anococcygeus, with a motor adrenergic innervation and an inhibitory innervation whose transmitter is unknown. The pharmacological properties of the cat muscle were investigated and compared with those of the rat muscle.2 The cat muscle contracts to noradrenaline, 5-hydroxytryptamine, tyramine, amphetamine, guanethidine, cocaine and lysergic acid diethylamide (LSD). The effects of noradrenaline and 5-hydroxytryptamine are blocked by phentolamine and methysergide respectively.3 The cat anococcygeus is relaxed by acetylcholine, carbachol, isoprenaline, ATP, prostaglandins E(1), E(2) and F(2alpha) and vasopressin, all of which contract the rat muscle. The effects of acetylcholine and carbachol are blocked by atropine and those of isoprenaline by propranolol.4 Field stimulation produces contraction of the cat anococcygeus, which is blocked by phentolamine and guanethidine but unaffected by hexamethonium, atropine or neostigmine.5 In the presence of guanethidine (10(-5)M), the tone of the muscle is raised and field stimulation produces relaxation of the muscle. These inhibitory responses are unaffected by phentolamine, hexamethonium, atropine or neostigmine.6 Neostigmine potentiates the effects of acetylcholine, but not of carbachol in relaxing the cat anococcygeus and in contracting the rat anococcygeus, but has no effect on either motor or inhibitory responses to field stimulation.7 Cold storage for up to eight days had little effect on either the motor response to noradrenaline or the motor or inhibitory response to field stimulation of the cat anococcygeus. Beyond eight days, the response to field stimulation diminishes more rapidly than the response to noradrenaline.
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PMID:The response of the cat anococcygeus muscle to nerve or drug stimulation and a comparison with the rat anococcygeus. 482 62

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

Intrinsic vascular responsiveness to norepinephrine, transmural electrical stimulation, 5-hydroxy-tryptamine, and vasopressin was studied in isolated helical cut strips of cystic artery (downstream branch of hepatic artery) from 120 subjects and related to blood pressure. Blood pressure, thickness of the tunica media, and passive elastic properties of arterial strips were each significantly correlated with age. With the exception of blood pressure in the female subjects, it is doubtful that these relationships are of major biologic significance. Nevertheless, in subgroup formation, care was taken to control for age. Hypertension was arbitrarily defined in three different ways as: (a) two diastolic pressure measurements greater than or equal to 90 mm Hg (HT90); (b) two diastolic pressure measurements greater than or equal to 95 mm Hg (HT95); or (c) treatment for hypertension instituted by a physician 6 months to 2 years after arteries were studied (HTQ). In arteries of hypertensive female subjects, responsiveness to norepinephrine (and possibly to 5-hydroxytryptamine) was increased significantly over the first half of the dose-response curve, particularly in the arteries of HT95 and HTQ subjects. Responses to transmural electrical stimulation and vasopressin were not consistently different. Such differences were not seen in arteries of male subjects where, if anything, responsiveness to norepinephrine (but not 5-hydroxytryptamine) was decreased. The present observations were made in the absence of any substantive difference in arterial dimensions (e.g., cross-section area) or in the maximal response to norepinephrine. The data support the notion that, at least for female subjects, alteration in intrinsic vascular responsiveness may play a role in the pathogenesis of human essential hypertension.
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PMID:Relationship of blood pressure to the responsiveness of an isolated human artery to selected agonists and to electrical stimulation. 608 64

The effects of noradrenaline and of raised external potassium ([K+]o) on the efflux of 86Rb or 42K and on tension were studied in preparations taken from eight different arteries under various conditions. There was a 10-fold variation in the maximum 86Rb efflux evoked by noradrenaline (10(-5)-10(-4) M) in the arteries studied, even though tension generated was comparable. Arterial contractions were either accompanied by large increases in 86Rb efflux, e.g. rabbit ear artery and aorta, guinea-pig and rabbit pulmonary artery, or by small increases, e.g. rabbit and guinea-pig mesenteric artery, rabbit brachial artery and guinea-pig abdominal aorta. Raising [K+]o also had a diverse effect on 86Rb and 42K efflux: arteries giving small increases in efflux to noradrenaline also gave small increases in efflux to raised [K+]o. The maximum efflux evoked by raised [K+]o was on average three times greater than the maximum efflux evoked by noradrenaline in the arteries studied. The heterogeneity of the efflux response could not be explained by the quantitative heterogeneity of the efflux response could not be explained by the quantitative differences in the effects of noradrenaline or of raised [K+]o on membrane potential or, in the case of noradrenaline, by differences in the alpha-receptors. In arteries in which the noradrenaline-evoked 86Rb efflux was small, histamine, 5-hydroxytryptamine, vasopressin and angiotensin also had little effect. Conversely, where noradrenaline produced a large increase in 86Rb efflux those other stimulants had comparable effects. Removal of extracellular calcium only slightly reduced the increment in 86Rb efflux evoked by 66 mM-external K+ in the rabbit aorta even though contractions were virtually abolished under these conditions. In the case of 10(-5) M-noradrenaline, 40% of the contraction remained and its effect on efflux was significantly increased (P less than 0.05) in calcium-free conditions. Essentially similar results were obtained using 42K. Tetraethylammonium (10-20 mM) produced a significant and substantial reduction (P less than 0.001) in the 86Rb efflux evoked by raised [K+]o while only slightly affecting the noradrenaline-evoked efflux in the rabbit aorta. It was concluded from these efflux experiments on vascular muscle that the channels through which potassium can escape, opened by depolarization and by activation of alpha-receptors with noradrenaline, are from different populations, and that their properties vary from one artery to another. We have been unable to detect any substantial calcium-activated component in 42K or 86Rb efflux responses to raised [K+]o or to noradrenaline.
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PMID:The diverse effects of noradrenaline and other stimulants on 86Rb and 42K efflux in rabbit and guinea-pig arterial muscle. 609 28

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