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. Alterations in vascular reactivity were assessed in isolated artificially perfused kidneys from stroke-prone spontaneously hypertensive (spSH) rats at different stages of hypertension and after neonatal sympathectomy with 6-hydroxydopamine (6-OHDA). 2. During the pre-hypertensive stage, and the early and chronic stages of hypertension, the responses to noradrenaline, vasopressin, serotonin and angiotensin II were enhanced in renal vascular beds from spSH animals compared with age- and sex-matched Wistar-Kyoto (WK) rats; dose-response curves were shifted to the left, had steeper slopes, greater maximal responses and decreased thresholds. 3. With increasing severity and duration of hypertension, renal vascular resistance at maximal vasodilatation increased, the slopes of the dose-response curves were steeper and maximal responses were greater. 4. Neonatal sympathectomy with 6-OHDA greatly attenuated but did not prevent the eventual development of hypertension; furthermore, this treatment had no effect on the enhanced resistance or reactivity in renal vascular beds from spSH rats. 5. The appearance of enhanced resistance and reactivity in the early stages of hypertension and the inability to prevent these vascular changes by neonatal sympathectomy suggest that these alterations are a primary pathogenic mechanism in spSH rats.
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PMID:Vascular reactivity in the pathogenesis of spontaneous hypertension. 54 Apr 70

1. In order to test whether the release of E-type prostaglandins from the kidney by various vasoconstrictor stimuli is related specifically to adrenoreceptor activation, we have compared release of prostaglandin E-like material from perfused rat kidneys during infusion of noradrenaline or vasopressin. 2. Concentrations of noradrenaline or vasopressin that produced comparable rises in renal perfusion pressure also released comparable amounts of prostaglandin E-like material. This effect was abolished by infusion of an inhibitor of prostaglandin synthesis into the kidney. 3. We conclude that liberation of E-type prostaglandins during renal vasoconstriction is probably related to the activation of intrarenal smooth muscle and odes not involve any specific hormonal receptor. Stimulation of release of prostaglandin E may explain certain reported renal actions of vasopressin.
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PMID:Release by vasopression of E-type prostaglandins from the rate kidney. 60 58

The administration of 5 I. U. oxytocin (by quick infusion) or of 5 I. U. vasopressin-lysine (intramuscularly) to healthy subjects was followed by a significant decrease in the plasma non-esterified fatty acid level. We regard this as evidence of inhibition of basal lipolysis in the adipose tissue. Vasopressin also completely blocked an increase induced in the plasma non-esterified fatty acid level by activating hormone-sensitive lipase in the adipose tissue by the infusion of 0.5 mg noradrenaline.
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PMID:Inhibition of lipolysis by oxytocin and vasopressin. 61 48

Pressor reactivity to noradrenaline or vasopressin was studied in unanaesthetized, pithed and isolated perfused hindquarter, preparations from renal and spontaneously hypertensive rats. Unanaesthetized renal and spontaneously hypertensive rats showed hyperreactivity to noradrenaline and vasopressin. Vascular responses of noradrenaline in pithed and isolated perfused hindquarter preparations were to a lesser extent but significantly greater in the renal hypertensive rat, while responses of pithed and isolated perfused hindquarter preparations to noradrenaline were within normal limits in the spontaneously hypertensive rat.
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PMID:Cardiovascular reactivity in renal and spontaneously hypertensive rats. 70 43

Dopamine and noradrenaline content in the posterior pituitary were found to be lower in alcohol-loaded unanesthetized rats than in rats thirsting for 72 h. Dopamine content was also found to be lower in anesthetized saline loaded rats in comparison with hydropenic animals. It is concluded that in situations in which an increase of vasopressin release is expected, the posterior pituitary content of catecholamines will also be increased, and vice versa, which might imply their role in the release of vasopressin.
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PMID:Posterior pituitary dopamine and noradrenaline content: effect of thirst, ethanol and saline load. 74 79

The effects of norepinephrine, phentalamine, oxytocin, vasopressin, several prostaglandins, and indomethacin on the spontaneous motility of isolated guinea pig cauda epididymidis were explored. Phentolamine and indomethacin reduced the isometric peak tension of spontaneous epididymal contractions. Phentolamine also depressed the frequency. Both findings suggest that catecholamines and endogenous prostaglandins are in some way regulators of the spontaneous motility of the cauda epididymidis. Norepinephrine resulted in the development of a distinct, sustained, tonic contraction without phasic activity, whereas prostaglandins E1, E2, and F2 alpha elicited a tonic increase accompanied by frequent, superimposed, phasic contractions. Both oxytocin and vasopressin comparably enhanced epididymal motility, producing contractile responses similar to those observed with prostaglandins. Since the epididymal contractions can influence the time spent by spermatozoa in passing through the ductus epididymidis, the above-mentioned compounds could play an important role in spermatozoal transport via modulation of epididymal contractile activity. In addition, such naturally occurring substances might regulate the release of sperm from the last portion of the epididymis into the ductus deferens.
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PMID:Physiologic and pharmacologic studies on the motility of isolated guinea pig cauda epididymidis. 80 41

1 The hepatic portal vein of the anesthetized dog was cannulated and perfused with blood derived from the cannulated superior mesenteric vein. 2 The portal vein was perfused at constant flow, the hepatic portal venous pressure being monitored continuously together with the inferior vena caval pressure. From these measurements, the hepatic portal venous vascular resistance was calculated. 3 Noradrenaline and adrenaline were injected intraportally in graded doses which caused dose-dependent increases in the hepatic portal vascular resistance. At all doses, adrenaline was significantly (P less than 0.05) more potent than noradrenaline. 4 Intraportal injections of vasopressin caused reductions in calculated hepatic portal venous vascular resistance in most experiments; three effects were dose-dependent. 5 No tachyphylaxis to the effects of noradrenaline, adrenaline or vasopressin was observed. 6 Intraportal injections of angiotensin caused dose-dependent increases in calculated hepatic portal vascular resistance up to 5 mug; therafter larger doses caused smaller increases in portal resistance. 7. Repeated intraportal injections of angiotensin revealed the existence of tachyphylaxis in the hapatic portal vascular bed. 8 Intraportal infusions of anagiotensin caused rises in calculated hepatic portal vascular resistance from which there was almost complete 'escape' despite the continued infusions. Infusions of noradrenaline which caused similar rises in calculated portal vascular resistance did not exhibit equivalent degrees of 'escape'. 9 The development of tachyphylaxisx explains the fact that doses of 10 and 20 mug of angiotensin injected after 5 mug doses produced smaller effects. If a much longer time interval was allowed between injections (30 min), the dose-response curve to angiotensin had a sigmoid shape. 10 These findings are discussed with respect to their possible importance in the functional status of the hepatic portal vascular bed in this species.
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PMID:The effects of intraportal injections of noradrenaline, adrenaline, vasopressin and angiotensin on the hepatic portal vascular bed of the dog: marked tachyphylaxis to angiotensin. 83 16

Clomipramine inhibited pressor responses to potassium ions and vasopressin in the rat mesenteric vascular bed with an ID50 of about 1.8 microgram/ml against both pressor agents and the actions of indomethacin and PG2 on the clomipramine effect suggested that the drug may have been antagonising the action of an endogenous PG. This was supported by the inhibitory action of clomipramine on PG2 actions on guinea-pig ileum. A lower concentration also inhibited pressor responses to noradrenaline and angiotensin (ID50 about 9 ng/ml): inhibition was increased by PG2 and reduced by indomethacin. In this preparation potassium and vasopressin act primarily by stimulating calcium entry from the extracellular fluid whereas noradrenaline and angiotensin act primarily by releasing calcium from intracellular or membrane-bound stores. Our results can be explained by two actions: 1. a PG-antagonist action of clomipramine at the cell membrane and 2. a selectve inhibitory effect on release of intracellular calcium. Clomipramine may prove useful in studying PG and calcium-dependent mechanisms.
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PMID:Actions of the tricyclic antidepressant clomipramine on responses to pressor agents. Interactions with prostaglandin E2. 89 8

The responsiveness of retinal vasculature to i.v. administration of several potent vasoactive agents was studied in pentobarbital anesthetized rats by taking fundus photographs. Since cerebral vasculature had been claimed to react in a similar manner but less liably than retinal vessels to some vasoactive substances, the findings were applied to the problem of reactivity of brain vessels. Sublethal doses of noradrenaline, adrenaline, 5-hydroxytryptamine, angiotensin amide and arginine orlysine vasopressin caused no marked acute ( less than or equal to 2 min) vasoconstriction in retinal vessels. Nor did any of these agents or bradykinin elicit vasodilatation. The late vasoconstriction (greater than 2 min) found in succumbing animals was most likely unspecific, since it did not occur until severe toxic symptoms appeared. The findings support the concept that intracerebral vessels are quite resistant to the direct action of many vasoactive agents given i.v.
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PMID:The poor reactivity of retinal vessels to systemic administration of vasoactive agents in pentobarbital anesthetized rats. 89 23

Responses of isolated helical strips of ovine ear artery to electrical stimulation of postganglionic adrenergic neurons and exogenous agonists were studied at various stages of development from 110 days of gestation through to adulthood. Only rudimentary responses were observed at 110-115 days of gestation. A parallel development of responses to noradrenaline (NA), serotonin, and lysine vasopressin began sometime after 110-115 days of gestation and continued until 133-137 days of gestation but there was little development of the latter responses until more than 3-5 days post partum. Development of responses to exogenous agonists was incomplete 2-3 weeks post partum. The development of postganglionic adrenergic responses lagged behind those to exogenous NA. Two to three weeks post partum the NA maximal response was one-third that of adult tissue whereas the response to 16 Hz (highest frequency used) was one-sixth that of adult tissue. The NA threshold concentration was lower in arterial strips of adult animals than it was in those of younger animals. The data suggest that development of functional post-ganglionic adrenergic innervation of vascular smooth muscle begins late in gestation and continues well after birth; this development is preceded by development of vascular mechanisms involved in the response to several agonists.
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PMID:Responses to electrical stimulation, noradrenaline, serotonin, and vasopressin in the isolated ear artery of the developing lamb and ewe. 92 79


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