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. The proposal that alpha,beta-methylene adenosine 5'-triphosphate (mATP) inhibits pressor responses in the pithed rat by selective desensitization of P2x-purinoceptors was examined by comparing the selectivity of its inhibitory effect on vascular responses in vitro and in vivo. 2. In isolated ring preparations of rat femoral and tail artery, which had been denuded of endothelium, mATP markedly reduced the contractile response to exogenous ATP but had no effect on the response of the arteries to exogenous noradrenaline (NA). 3. In the pithed rat a substantial proportion of the pressor response to sympathetic nerve stimulation was resistant to alpha-adrenoceptor blockade, suggesting a non-adrenergic component to the sympathetic vasoconstriction. 4. In the pithed rat, repeated administration of desensitizing doses of mATP attenuated the pressor response to sympathetic nerve stimulation by approximately 80%, suggesting that a component of the sympathetic vasoconstriction is mediated by ATP acting on vascular P2x-purinoceptors. However, the same mATP treatment also attenuated, to a similar degree, the pressor responses to intravenous NA, angiotensin II and vasopressin, indicating that the desensitization procedure was non-selective. 5. These results demonstrate that while mATP can be used to desensitize selectively P2x-purinoceptors in vitro, its attenuation of the sympathetic nerve-mediated pressor response in vivo is non-selective.
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PMID:Investigation of the selectivity of alpha, beta-methylene ATP in inhibiting vascular responses of the rat in vivo and in vitro. 197 97

To study the haemodynamic and neurohumoral effects of nisoldipine (2 X 10 mg) vs captopril (3 X 25 mg), 24 patients with heart failure (New York Heart Association class II and III) due to coronary artery disease were treated in a randomized double-blind trial over 3 months. Both drugs were well tolerated. Clinical status was similarly improved in both groups, nisoldipine exerted an additional antiischaemic effect. Nisoldipine lowered the mean arterial pressure and capillary wedge pressure acutely and also after long-term treatment. The increase in cardiac index and stroke volume index, however, which was pronounced after acute administration, was no longer present after 3 months of therapy at rest and was abolished during exercise. Norepinephrine plasma concentration increased after the first dose, plasma renin activity did not change, and aldosterone plasma concentration showed a small insignificant decrease. Urine concentrations of norepinephrine and vasopressin were slightly elevated after the 3-month therapy. After captopril, mean arterial pressure and pulmonary capillary wedge pressure decreased acutely and at follow up. Cardiac index and stroke volume index increased significantly only during exercise at follow-up. Plasma renin activity was significantly elevated and aldosterone plasma concentration only slightly lowered. In contrast to what was seen with nisoldipine, plasma norepinephrine concentration and urine catecholamine and vasopressin concentrations remained unchanged. In conclusion, the pronounced haemodynamic effects seen after the first dose of nisoldipine are mostly abolished after long-term treatment, probably due to neurohumoral counterregulation. The haemodynamic response to captopril is complete only after long-term treatment, without evidence of activation of the neurohumoral systems.
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PMID:Acute and long-term haemodynamic and neurohumoral response to nisoldipine vs captopril in patients with heart failure: a randomized double-blind study. 168 8

The effects of quinpirole, a specific dopamine D2 receptor agonist, were investigated on cardiovascular responses and plasma levels of catecholamines and vasopressin in two groups of conscious dogs: (1) control dogs and (2) dogs with diabetes insipidus (i.e. animals surgically deprived of vasopressin). In normal dogs, i.v. quinpirole (30 micrograms/kg) elicited a decrease in blood pressure associated with a rise in both plasma catecholamine and vasopressin levels. In dogs with diabetes insipidus, i.v. quinpirole induced a more marked decrease in blood pressure than in normal dogs. Quinpirole did not change plasma noradrenaline and vasopressin levels in dogs with diabetes insipidus. The present study demonstrates that the decrease in blood pressure elicited by quinpirole is associated with an increase in vasopressin release, which counteracts the hypotensive effect of the the dopamine D2 receptor agonist.
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PMID:Involvement of vasopressin in the cardiovascular effects of quinpirole. 197 26

1. Intravenous infusions of UK14304 (0.3-10 micrograms/kg per min) in pithed rat produced dose-dependent pressor responses which were not affected by prazosin (10 micrograms/kg) but were reduced by yohimbine (0.3 mg/kg). 2. Pressor responses to noradrenaline (0.1 micrograms/kg), phenylephrine (1 micrograms/kg) and vasopressin (10 mU/kg) were enhanced during infusions of UK14304 (0.03-1 micrograms/kg per min). Likewise, pressor responses to spinal sympathetic stimulation were enhanced during infusions of low concentrations of UK14304 (0.03-0.3 microgram/kg per min) but were reduced during infusion of a higher concentration of UK14304 (10 micrograms/kg per min). 3. After administration of yohimbine (0.3 mg/kg) or the calcium channel blocking drug diltiazem (infused at 50 micrograms/kg per min), pressor responses to noradrenaline and UK14304 were reduced, and responses to noradrenaline during infusion of UK14304 were not enhanced. 4. Prazosin (10 micrograms/kg) revealed a secondary depressor component in the response to sympathetic stimulation which is due to beta-adrenoceptor activation, since it was abolished by ICI 118551 (0.3 mg/kg). In the presence of ICI 118551 plus prazosin, pressor responses to sympathetic stimulation were enhanced during infusions of UK14304. 5. The depressor response to nitroprusside and the depressor component of responses to sympathetic stimulation after prazosin were enhanced during infusions of UK14304 at concentrations that increased the blood pressure. 6. The findings show that alpha 2-adrenoceptor activation enhanced the pressor responses to sympathetic nerve stimulation, noradrenaline, phenylephrine and vasopressin in the pithed rat and beta-adrenoceptor activation produced depressor responses which increased with increasing blood pressure.
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PMID:Effects of the alpha 2-adrenoceptor agonist UK14304 on pressor responses in pithed rats. 198 Feb 35

1. Effects of vasoactive substances were investigated in the canine isolated spinal branch of the intercostal artery (SBICA). 2. Addition of angiotensin II (AII), vasopressin, noradrenaline (NA), adrenaline, 5-hydroxytryptamine (5-HT), and dopamine each produced concentration-dependent contraction in the SBICA, whereas prostaglandin F2 alpha, histamine, and tyramine caused only slight contraction. The decreasing order of the potency of contractile agents was AII much greater than vasopressin = NA greater than 5-HT greater than adrenaline much greater than dopamine. 3. Although the pD2 value for phenylephrine (5.31 +/- 0.36) was smaller than that for NA (6.48 +/- 0.13), there was no significant difference in Emax value between these two agonists in the SBICA. On the other hand, xylazine produced only a slight contraction, the pD2 value being 3.59 +/- 0.08. Phentolamine (10(-8)-10(-6) M) and prazosin (10(-8)-10(-6) M) competitively inhibited the NA-induced contraction, while yohimbine (10(-8)-10(-6) M) did not. 4. Acetylcholine (ACh), sodium nitroprusside (SNP), ATP, ADP, and adenosine caused concentration-dependent relaxations in SBICA following contraction with NA. On the other hand, isoprenaline up to 10(-4) M did not produce any relaxation. The decreasing order of potency of the relaxant agents was ACh greater than SNP much greater than ATP = ADP = adenosine. 5. The ACh-induced relaxation was competitively inhibited by atropine and was abolished by mechanical removal of the endothelium. Aspirin (5 x 10(-5) M) did not affect the relaxant response to ACh, while oxyhaemoglobin (10(-5) M) and methylene blue (10(-5) M) produced significant attenuation. 6. These results suggest that NA produces contraction of the isolated canine SBICA which is mainly mediated via alpha 1-adrenoceptors and that ACh causes a relaxation of the SBICA due to release of endothelium-derived relaxing factor (EDRF) from the endothelial cells.
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PMID:Contractile and relaxant responses of the canine isolated spinal artery to vasoactive substances. 198 Aug 36

In addition to the classical transmitters noradrenaline and acetylcholine, other transmitters have been identified in perivascular nerves, including 5-hydroxytryptamine, ATP and a number of peptides. This paper discusses pre- and postjunctional neuromodulation of vascular transmission, and cotransmission involving noradrenaline, ATP and neuropeptide Y in sympathetic nerves, acetylcholine and vasoactive intestinal polypeptide in parasympathetic nerves, and substance P, calcitonin gene-related peptide and ATP in 'sensory-motor' nerves. Vasomotor nerves derived from intrinsic neurones, for example in the heart and gut, are also discussed. Subpopulations of endothelial cells store and release a variety of substances, including acetylcholine, substance P, ATP, 5-hydroxytryptamine, vasopressin and angiotensin II, that act on receptors on endothelial cells and lead to the production of endothelium-derived relaxing factor (identified as nitric oxide) which, in turn, produces vasodilation in response to changes in flow and hypoxia. Endothelium-derived contracting factors such as endothelin may also be released. There appears to be a resting dynamic balance between endothelium-derived vasodilator tone and sympathetic vasoconstrictor tone, which is altered under different physiological and pathophysiological circumstances. Long-term (trophic) interactions between perivascular nerves and endothelial cells are discussed, as are the changes in vascular control mechanisms that occur with ageing and hypertension and in the nerves that remain following trauma or surgery.
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PMID:Local mechanisms of blood flow control by perivascular nerves and endothelium. 198 71

In the isolated perfused rat tail artery, the alpha 2-adrenoceptor agonist UK14304 alone did not exert a direct vasoconstrictor action until a concentration of at least 30 microM was reached. However, when administered during the sustained vasoconstrictor response to 1.6 microM vasopressin, UK14304 (1-100 nM) produced additional concentration-dependent increases in perfusion pressure. The vasoconstrictor response to UK14304 in the presence of vasopressin was antagonized by idazoxan (1 microM) but was not affected by prazosin (10 nM), indicating that it was due to activation of alpha 2-adrenoceptors, and it was reduced by diltiazem (10 microM) and abolished when perfusion was done with a Ca2(+)-free solution, suggesting that the effect depends on the influx of Ca2+. UK14304 (50 nM) also produced a further increase in perfusion pressure when given during sustained vasoconstrictor responses to phenylephrine (1 microM) or low concentrations (100 nM) of noradrenaline or serotonin. However, UK14304 did not produce a further increase in perfusion pressure when given during sustained vasoconstrictor responses to higher concentrations (300 nM) of noradrenaline or serotonin: the lack of an additional effect of UK14304 was not due to the primary response to noradrenaline or serotonin being maximal. The findings show that vasoconstrictor responses following activation of alpha 2-adrenoceptors may be uncovered by an increase in vascular tone produced by some agonists.
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PMID:Vasoconstrictor responses to the alpha 2-adrenoceptor agonist UK14304 during responses to noradrenaline, phenylephrine, serotonin and vasopressin of the rat tail artery. 198 65

After completion of abdominal aortic graft, 29 patients received an i.v. infusion of placebo (n = 16) or clonidine 7 micrograms kg-1 (n = 13) over 120 min in a double-blind study. Cardiovascular variables were measured and plasma samples obtained up to 5 h after arrival in the recovery room, for assay of noradrenaline, adrenaline, vasopressin and renin concentrations. Noradrenaline, adrenaline and vasopressin concentrations decreased in the clonidine group throughout recovery (P less than 0.001, 0.05 and 0.05, respectively, vs placebo). Heart rate was less in the clonidine group (P less than 0.01). There was no significant difference in mean arterial pressure between groups. Stroke volume was larger (P less than 0.01) and there were fewer episodes of hypertension (P less than 0.05) and tachycardia in the clonidine group. In addition, a reduction in the number of circulatory interventions (P less than 0.05) and episodes of shivering was noted in the clonidine group. Mean (SD) postoperative volume requirements were larger in the clonidine group (total postoperative input: clonidine 1462 (604) ml; placebo 1064 (348) ml (P less than 0.05]. These data are consistent with the observation that clonidine modifies endocrine and circulatory status after major surgery.
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PMID:Effect of clonidine on the circulation and vasoactive hormones after aortic surgery. 199 45

Acute fetal hypoxemia increases the vascular resistance of the umbilical veins as well as that of the liver. Because, at least in the human, the umbilical-placental circulation has no autonomic innervation, circulating hormones could well be responsible for this increase in umbilical-placental outflow resistance. In chronically instrumented fetal sheep, norepinephrine, epinephrine, vasopressin, and angiotensin II were infused in sequentially increasing doses into the descending aorta and vascular resistance to umbilical-placental blood flow was measured. Norepinephrine and epinephrine increased the vascular resistance of the umbilical veins in a dose-dependent manner. Both catecholamines also increased the vascular resistance of the liver, resulting in an increase in ductus venosus blood flow. In contrast, vasopressin and angiotensin II had no effect on umbilical-placental outflow resistance. Thus catecholamines may be responsible for the increase in the vascular resistance of the umbilical veins and liver in response to acute fetal hypoxemia.
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PMID:Umbilical and hepatic venous responses to circulating vasoconstrictive hormones in fetal lamb. 201 24

The effects of the vasodilator drugs hydralazine, labetalol, prazosin, and nitrendipine were studied on responses to K+ (124 mmol/L), noradrenaline, vasopressin, and angiotensin II in small human maternal intramyometrial arteries and on responses to K+, prostaglandin (PG) F2 alpha, and angiotensin II in fetal stem villous arteries. The vessels were dissected from biopsy specimens obtained during term cesareans and mounted in organ baths. Hydralazine failed to inhibit responses to any of the agonists tested in the fetal and maternal arteries. Labetalol and prazosin decreased responses to noradrenaline but did not affect contractions induced by the other agonists in maternal arteries. In fetal arteries, which did not respond to noradrenaline, no effects of labetalol and prazosin were found. Nitrendipine inhibited responses to all the agonists tested in maternal arteries. In fetal preparations, the drug decreased responses to K+ and PGF2 alpha but did not affect contractions induced by angiotensin II. Vasodilator drugs applied for treatment of pregnancy-induced hypertension show differential effects on human maternal and fetal uteroplacental arteries, depending on their mode of action and the agonists responsible for the contractile activation in these vessels.
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PMID:Effects of vasodilators on isolated human uteroplacental arteries. 201 93


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