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 effects of local intra-arterial infusions of serotonin (5 or 25 micrograms base/min) or norepinephrine (1 or 5 micrograms base/min) on cutaneous (skin) and skeletal muscle vasculatures were investigated in canine forelimbs perfused at constant flow in dogs anesthetized with pentobarbital. Norepinephrine produced dose-related constriction of the skin and skeletal muscle vasculatures. In the cutaneous vascular circuit, norepinephrine produced large artery, small vessel, and large vein constriction. The increase in cutaneous vascular resistance was primarily due to an increase in small vessel resistance. Serotonin did not increase skeletal muscle vascular resistance but produced marked cutaneous vasoconstriction subsequent to large artery and large vein constriction. The small vessels, if anything, tended to dilate. The skin and skeletal muscle vascular responses to serotonin and norepinephrine were similar in innervated and acutely denervated forelimbs. Phentolamine pretreatment completely blocked all vascular actions of norepinephrine, and largely inhibited the cutaneous vasoconstriction produced by the infusion of the low dose of serotonin. However, the cutaneous large artery and large vein constriction produced by the infusion of the high dose of serotonin was not affected by phentolamine pretreatment. Cyproheptadine pretreatment blocked or largely inhibited the cutaneous vasoconstriction produced by serotonin only in doses which also inhibited norepinephrine and vasopressin cutaneous vasoconstriction. Pretreatment with methysergide blocked or largely inhibited the cutaneous large artery and large vein constriction produced by infusions of serotonin. Norepinephrine and vasopressin produced significant vasoconstriction in the presence of methysergide. These data suggest that the cutaneous large artery and large vein constriction produced by serotonin is not due to the activation of postjunctional alpha-adrenergic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence that serotonin receptors mediate the cutaneous vasoconstriction produced by 5-hydroxytryptamine in canine forelimbs. 662 7

The extramural artery of the human gall bladder (cystic artery), a small artery (outside diameter 1.3 +/- 0.03 mm) with a thick muscular wall and little elastin within the tunica media, has catecholamine fluorescence localized to the adventitia-medial border. Isolated helical strips of the artery are responsive to norepinephrine (NE), 5-hydroxytryptamine (5HT) and vasopressin (VP) at low concentrations, but at the maximal frequency of transmural electrical stimulation used (16 Hz), the response is only 10--20% of the NE maximum response. Phentolamine (2.7 X 10(-6) M) antagonized responses to NE, 5HT and, to a lesser degree, electrical stimulation and these actions are similar to those reported in other mammalian tissue. In vitro use of reserpine (1.6 X 10(-5) M) and guanethidine (4 X 10(-5) M) also produced effects which were predictable from effects observed in other mammalian tissues; except reserpine diminished responsiveness to NE and 5HT and guanethidine enhanced responses to the early administered electrical stimulation.
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PMID:Isolated human cystic artery: responses to common agonist and antagonist drugs. 720 97

Increased neurotransmitter release during sympathetic nerve stimulation may contribute importantly to the maintenance of spontaneous hypertension. Therefore, transmitter release and vascular reactivity were measured in perfused mesenteric vasculature of spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto rats (WKY). Increase in norepinephrine release, measured as total tritium overflow, during periarterial nerve stimulation was significantly greater in SHR than in WKY, as was the vasoconstrictor response. Even after blockade of neuronal uptake with cocaine (10 microM), or of neuronal as well as extraneuronal uptake with cocaine plus metanephrine (20 microM), norepinephrine overflow was still greater in SHR than in WKY. The greater vasoconstrictor response in SHR still persisted following uptake blockade. Phentolamine (5.3 microM) increased transmitter overflow markedly but equally in both SHR and WKY thereby suggesting that increased transmitter release in SHR was not due to alterations in presynaptic alpha-adrenoceptor mechanism. Vascular reactivity not only to periarterial nerve stimulation but also to norepinephrine, vasopressin, and barium chloride was increased in SHR. These results suggest that, in SHR, increases in norepinephrine release as well as vasoconstrictor reactivity contribute to the maintenance of hypertension.
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PMID:Sympathetic nerve function and vascular reactivity in spontaneously hypertensive rats. 730 83

1 The response of the dog anococcygeus muscle to field stimulation and to some drugs has been studied. The results are compared with those reported previously in the rat, cat and rabbit. 2 Field stimulation produced frequency-dependent contractions which were inhibited by guanethidine and phentolamine. When the tonus of the muscle was increased with guanethidine, field stimulation always produced frequency-dependent relaxation. The relaxation was not prevented by propranolol. 3 The muscle was contracted by noradrenaline, tyramine, acetylcholine, histamine (H1), 5-hydroxy-tryptamine, prostaglandin E2 and vasopressin. Phentolamine, atropine, promethazine (but not cimetidine) and methysergide inhibited the effect of the respective agonists. 4 After increasing the tonus of the muscle, it was relaxed by low concentrations of isoprenaline. The relaxation was antagonized by propranolol. 5 The response to adenosine triphosphate (ATP) was variable. In some preparations, it relaxed the muscle, in others it contracted the muscle prior to relaxation, in others still it only contracted the muscle. Indomethacin did not prevent ATP-induced contraction. 6 It is concluded that the anococcygeus of the dog, like that of rat, cat and rabbit, has an adrenergic motor innervation and an inhibitory innervation, the transmitter of which is not identified.
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PMID:Pharmacological study of the anococcygeus muscle of the dog. 747 Jul 46

The modulation of the production of prostacyclin and thromboxane from cat and cat aortic tissue slices by different vasoactive agents has been studied in order to reveal whether the release of these main two vasoactive prostanoids goes in parallel or may be controlled independently. Norepinephrine, isoproterenol, phentolamine, propranolol, angiotensin II, vasopressin, bradykinin, thrombin, verapamil, gallopamil, dopamine or methionin enkephalin were added to the incubation medium and 6-keto-PGF1 alpha (the stable metabolite of prostacyclin) and TxB2 (the stable metabolite of thromboxane) were determined in the supernatant by radioimmunoassay. The ratio of the release of prostacyclin and thromboxane was computed. Norepinephrine increased both prostacyclin and thromboxane release. Isoproterenol increased the ratio of prostacyclin and thromboxane released in cat aortic tissue slices. Phentolamine and propranolol had no effects. Angiotensin II induced a slight but statistically insignificant increase in the ratio of the two prostanoids released. Vasopressin increased thromboxane release only. Bradykinin stimulated the prostacyclin while thrombin stimulated the thromboxane release. Verapamil decreased both prostacyclin and thromboxane production. Gallopamil decreased prostacyclin release and increased thromboxane release from vessel wall slices in a certain concentration range causing a characteristic dose dependent minimum in the ratio of prostacyclin and thromboxane release. Dopamine separately increased prostacyclin release while enkephalin had no significant effect. The data obtained show that in vascular tissue some unidentified yet cytophysiological mechanisms might exist which specifically control the activities of the prostacyclin synthase and thromboxane synthase enzymes.
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PMID:Prostacyclin and thromboxane production of rat and cat arterial tissue is altered independently by several vasoactive substances. 890 22

1. The effects of fetal intravenous treatment with phentolamine or a vasopressinergic V1-receptor antagonist on the fetal cardiovascular responses to acute hypoxaemia in the llama were investigated. 2. Six llama fetuses were surgically prepared between 60 and 70 % of gestation under general halothane anaesthesia with vascular catheters and transit-time ultrasonic flow probes around a carotid artery and a femoral artery. At least 4 days after surgery all fetuses were subjected to a 3 h experiment: 1 h of normoxia, 1 h of hypoxaemia and 1 h of recovery while on slow i.v. infusion with saline. On separate days this experiment was repeated with fetal i.v. treatment with either phentolamine or a V1-receptor antagonist dissolved in saline. 3. During saline infusion all llama fetuses responded to acute hypoxaemia with intense femoral vasoconstriction. Phentolamine during normoxia produced hypotension, tachycardia and vasodilatation in both the carotid and the femoral circulations. During hypoxaemia, fetuses treated with phentolamine did not elicit the pronounced femoral vasoconstriction and all died within 20 min of the onset of hypoxaemia. A V1-receptor antagonist produced a femoral vasodilatation during normoxia but did not affect the fetal cardiovascular responses to acute hypoxaemia. 4. In conclusion, alpha-adrenergic and V1-vasopressinergic mechanisms contribute to a basal vasoconstrictor tone in the femoral circulation in the llama fetus. The enhanced femoral vasoconstriction during acute hypoxaemia in the llama fetus is not mediated by stimulation of V1-vasopressin receptors, but is dependent on alpha-adrenergic receptor stimulation. Such alpha-adrenergic efferent mechanisms are indispensable to fetal survival during hypoxaemia in the llama since their abolition leads to cardiovascular collapse and death.
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PMID:Adrenergic and vasopressinergic contributions to the cardiovascular response to acute hypoxaemia in the llama fetus. 992 92

Previous studies show that the choroid can maintain its blood flow despite changes in perfusion pressure, behaviour possibly mediated by an autoregulatory mechanism. However, the choroid's rich autonomic innervation suggests possible neural involvement in the response. To evaluate the potential neural contribution, choroidal blood flow was measured by laser Doppler flowmetry over a wide range of perfusion pressure before and after ganglionic blockade in anaesthetized rabbits. Although an upward shift in the pressure-flow (P-F) curve was anticipated due to loss of adrenergic tone, ganglionic blockade shifted the P-F curve downward, prompting a search for a neural vasodilator to explain the response. Cholinergic blockade with atropine failed to alter the P-F curve suggesting little parasympathetic involvement. By contrast, inhibition of nitric oxide (NO) synthase with nitro-L-arginine methyl ester (L-NAME) caused a dramatic downward shift in the P-F curve, suggesting the nitridergic nerves as the source of vasodilatory tone. However, the downward shift in the P-F curve with L-NAME was greater than seen with ganglionic blockade, indicating that endothelial NO rather than neural dilator tone predominates. Moreover, calcium channel blockade after L-NAME reversed the downward shift in the P-F curve suggesting that choroidal vascular tone is modulated by an interaction between NO and an unknown vasoconstrictor. Neither hexamethonium, losartan or a vasopressin antagonist given after L-NAME reversed the downward shift in the P-F curve, ruling out a neural vasoconstrictor, angiotensin II and vasopressin as the source of constrictor tone. Phentolamine given after L-NAME caused a small but significant reversal of the downward shift in the P-F curve, suggesting a minor adrenergic contribution. By contrast, the non-selective endothelin antagonist, A-182086, given after L-NAME significantly attenuated the choroidal constriction. These results indicate that an unknown neural dilator and locally produced NO and endothelin exert competing influences on the inherent reactivity of the choroidal resistance vessels as they respond to changes in perfusion pressure, and that this local regulation is likely modulated by extrinsic neurohumoral factors that are relatively quiet in the anesthetized rabbit.
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PMID:Modulation of choroidal autoregulation in the rabbit. 1050 75


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