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)

Effect of chronic angiotensin converting enzyme blockade on the pressor response to exogenous angiotensin II, noradrenaline and vasopressin were evaluated in DOCA-salt induced hypertensive rats using teprotide. The blood pressure of rats receiving teprotide chronically was reduced markedly. The pressor responses to exogenous angiotensin II was accentuated, while that of noradrenaline and vasopressin were significantly reduced. It is concluded that besides the angiotensin converting enzyme blocking action, the decrease in sensitivity of the pressor response to noradrenaline and vasopressin may contribute towards the antihypertensive activity of teprotide given chronically.
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PMID:Effect of chronic angiotensin-converting enzyme blockade on pressor responses to exogenous angiotensin II, noradrenaline and vasopressin in deoxycorticosterone acetate salt (DOCA)-induced hypertensive rats. 609 11

This study investigates the endogenous kallikrein-kinin system's role as a modulator of vasopressin action in the toad urinary bladder. Kalli-krein inhibition by aprotinin, which results in decreased kinin production, significantly increased both vasopressin and 8-Br-cyclic (c) AMP-stimulated water flow. Kinin potentiation by the kininase II inhibitor captopril (SQ 14225) significantly decreased vasopressin and 8-Br-cAMP-stimulated water flow. In contrast to water flow, vasopressin-stimulated urea permeability was decreased by aprotinin and increased by captopril. We conclude that the endogenous kallikrein-kinin system represents a significant modulator of vasopressin action and it permits separate control of vasopressin-stimulated water flow and solute transport.
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PMID:Role of the endogenous kallikrein-kinin system in modulating vasopressin-stimulated water flow and urea permeability in the toad urinary bladder. 616 39

It has become increasingly clear that the potent vasoactive peptides bradykinin and angiotensin share a common point of metabolism, i.e., angiotensin-converting enzyme or kininase II, and may interact with prostaglandins to regulate regional blood flow. To establish whether the sensitivity to exogenous bradykinin was affected by the presence of angiotensin, vasodepressor dose-response curves to injected bradykinin were performed in conscious rats before and during a 1-h infusion of angiotensin I (30 ng/min), angiotensin II (30 and 300 mg/min), and [Sar2,Ala8]angiotensin II (5 micrograms/min). All of these induced a parallel leftward shift of the bradykinin dose-response curve of approximately threefold. No similar changes were observed during control infusions of dextrose, similar pressor doses of lysine vasopressin, or norepinephrine. Sensitivity to bradykinin was enhanced by saralasin in normal and nephrectomized rats, suggesting that the antagonist itself was responsible. Similar potentiation was present during both acute (1 h) and chronic infusions (9 days) of angiotensin II and attenuated the effect of a converting-enzyme inhibitor on bradykinin sensitivity. Accordingly, these results suggest a competitive interaction in vivo between angiotensin congeners and bradykinin at a point of bradykinin degradation, probably angiotensin-converting enzyme or kininase II. This is a potential additional mechanism by which these systems may interact to affect regional blood flow and must be considered in the interpretation of results obtained during saralasin infusion.
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PMID:Evidence for bradykinin potentiation by angiotensin congeners in conscious rats. 625 51

The activity of the angiotensin-converting enzyme (ACE) (kininase II, EC 3.4.15.1) was examined in 5 discrete hypothalamic nuclei of rats lacking vasopressin (homozygous Brattleboro rats, DI, di/di) and their corresponding controls (heterozygous Brattleboro rats, HZ, di/+, and Long Evans, LE, +/+ rats), with and without hormonal replacement with arginine-vasopressin (AVP). DI rats showed a vasopressin-reversible increased ACE activity when compared with LE controls, HZ rats showing intermediate activity. These changes occurred only in the supraoptic and periventricular hypothalamic nuclei, and were absent in other hypothalamic areas studied, including the paraventricular nucleus. These results provide biochemical evidence in support of previous anatomical and physiological data, for an interaction between the brain vasopressin and angiotensin systems in discrete hypothalamic nuclei, and suggest that vasopressin could regulate the formation of brain angiotensin II by modulating the activity of the converting enzyme.
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PMID:Vasopressin-reversible increase in angiotensin-converting enzyme in specific hypothalamic nuclei of Brattleboro rats. 628 72

The relationship of the vascular effect of captopril to angiotensin converting enzyme activity and prostaglandin-dependent mechanism was studied in rat isolated kidneys, perfused with Krebs-Henseleit at 20 ml/min per 2 kidneys, with basal perfusion pressures of 78 +/- 1 mm Hg (Mean +/- S.E.M.). Two doses of captopril were used; both low (0.05 microgram/ml) and high doses (5 microgram/ml) inhibited maximally the vasoconstrictor responses to 100 and 200 ng of angiotensin I. Captopril at the low dose did not affect the renal vasoconstrictor responses to norepinephrine (NE) (25-400 ng), whereas high-dose reduced the vasoconstriction to all doses of NE. Treatment with captopril tended to diminish dose-related release of prostaglandins in response to NE. Indomethacin (1 microgram/ml) prevented NE-induced release of bioassayable and radioimmunoassayable prostaglandins but did not affect the ability of captopril to reduce NE-induced vasoconstriction. High-dose captopril also decreased the vascular reactivity to angiotensin II (5 ng) and lysine vasopressin (10 mU); however, the renal vasoconstriction caused by PGE2 (80 ng) was unaffected by captopril. We conclude that high-dose captopril decreased vascular reactivity by a mechanism independent of converting enzyme inhibition and unrelated to a prostaglandin-dependent vascular mechanism.
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PMID:Captopril decreases vascular reactivity independently of changes in converting enzyme activity and prostaglandin release in the rat isolated kidney. 629 42

The role of vasopressin, the renin system, and sympathetic activity in sustaining blood pressure in the dehydrated state was investigated in normotensive nonanesthetized male Wistar rats. After 48-h dehydration, plasma arginine vasopressin was 14.0 +/- 1.7 pg/ml and plasma norepinephrine 0.46 +/- 0.05 ng/ml. In another group of rats in which the angiotensin converting enzyme inhibitor (MK 421, 5 mg po twice daily) was administered throughout the dehydration period, blood pressure was reduced by more than 20% (P less than 0.001), and both plasma arginine vasopressin and norepinephrine were higher at 23.4 +/- 3.9 pg/ml (P less than 0.01) and 0.83 +/- 0.07 ng/ml (P less than 0.01), respectively. Taken together, in rats with or without converting enzyme blockade, there was an inverse correlation between mean blood pressure and plasma arginine vasopressin (r = 0.67, P less than 0.01) as well as plasma norepinephrine (r = 0.82, P less than 0.01) levels. The acute administration of a specific vasopressin pressor inhibitor (dPVDAVP) reduced mean blood pressure in the rats with a blocked renin system by 16.9 mmHg (P less than 0.001). In rats without converting enzyme inhibition, the induced fall was only 6.4 mmHg. These results indicate that following 48-h dehydration the renin angiotensin system interacts with the vasopressin secretory mechanism to sustain blood pressure, with renin playing a predominant role. They further suggest that, following blockade of the renin system, activation of the sympathetic nervous system probably also contributes to blood pressure maintenance.
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PMID:Blood pressure maintenance in awake dehydrated rats: renin, vasopressin, and sympathetic activity. 630 21

We studied the activity of angiotensin I converting enzyme (ACE, kininase II, E.C. 3.4.15.1) in discrete areas of the brainstem and limbic system, and in circumventricular organs, pineal gland and choroid plexus of homozygous Brattleboro rats (DI) which are characterized by vasopressin deficiency and diabetes insipidus, with or without vasopressin replacement. We also determined ACE activity in heterozygous Brattleboro (HZ) and Long-Evans (LE) control rats. We found changes in ACE activity in several brain areas and the pineal gland of Brattleboro rats. ACE activity was increased in DI rats with respect to HZ and LE controls in the A1 area of the brainstem, locus coeruleus, and triangular nucleus of the septum. ACE activity in the A2 area of the brainstem, the nucleus tractus spinalis nervi trigeminii and the pineal gland was enhanced in both HZ and DI rats with respect to that of LE controls, but was not different between HZ and DI rats. ACE activity did not change in the other extrahypothalamic areas studied. The elevated ACE activity in extrahypothalamic areas of DI rats was not reversed by vasopressin replacement. These results suggest that a relationship between central vasopressin and angiotensin or bradykinin systems may exist in selective extrahypothalamic areas of the rat brain, and that peripherally administered vasopressin cannot influence this relationship.
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PMID:Selective increase of angiotensin-converting enzyme activity in discrete extrahypothalamic areas of Brattleboro rats. 631 41

Three structurally different drugs, MK421, SA446 and captopril, are angiotensin converting enzyme inhibitors. They induced a significantly greater fall in systolic blood pressure in sodium depleted rats than in sodium repleted ones. The combined administration of vasopressin or norepinephrine with MK421 eliminated the hypertensive effect of vasopressin or norepinephrine. Urinary kallikrein and kinin excretion were increased by MK421, SA446 or captopril in the sodium depleted rats whereas any significant changes in them were not observed in the sodium repleted rats. The combined administration of norepinephrine with MK421 induced further increases in urinary kallikrein and kinin excretion when compared to rats infused with norepinephrine alone, whereas the combined administration of vasopressin with MK421 did not induce any changes in them when compared to rats infused with vasopressin alone. Chronic infusion of captopril for up to 6 days in the rats induced a reduction of the vascular response to exogenous bradykinin; the blood pressure fall was less than that of the controls by 17% on Day 2 and by 18% on Day 6. These results indicate that the hypotensive response to angiotensin converting enzyme inhibitors was in part associated with the enhanced renal and vascular smooth muscle kallikrein-kinin system.
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PMID:Responses of the kallikrein-kinin system to angiotensin converting enzyme inhibitors in the rat. 632 15

The specificity of pepstatin A as an inhibitor of the cardiovascular actions of renin injected into anaesthetized rats has been investigated. Pepstatin A 70 micrograms/kg/min partially inhibited the pressor response to injected renin without affecting the pressor responses to injected angiotensin II, phenylephrine or vasopressin. Pepstatin A 150 micrograms/kg/min also produced partial inhibition of injected renin, but in addition caused significant inhibition of the other pressor agents. This was in contrast to the effects of the angiotensin converting enzyme inhibitor captopril, 100 micrograms/kg i.v., which caused greater inhibition of the renin pressor response than pepstatin A without affecting the pressor response to injected angiotensin II, phenylephrine or vasopressin. Finally the direct acting vasodilator hydralazine was found to have a similar non-specific inhibitory effect to pepstatin A on the pressor responses to injected pressor agents. It is concluded that pepstatin A reduces the pressor responsiveness to injected pressor agents and that this non-specific cardiovascular activity limits the usefulness of pepstatin A as a pharmacological tool to inhibit renal renin in vivo.
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PMID:Non-specific inhibition of pressor agents in vivo by the renin inhibitor pepstatin A. 639 34

We have studied the mechanisms contributing to the characteristic cardiovascular response produced after lesions of the A1 noradrenaline cell area in the ventrolateral medulla of the rabbit, at and below the level of the obex. Forty-five minutes after the A1 lesions there were dramatic increases in plasma adrenaline and plasma vasopressin (AVP) levels, which rose more than forty-fold, accompanied by smaller increases in plasma noradrenaline concentration and plasma renin activity (PRA) which were approximately doubled. Administration of an AVP antagonist did not effect the pressor response to A1 lesions but did reduce the bradycardia whereas administration of phentolamine, an alpha adrenoceptor blocker, completely prevented the increase in blood pressure after lesions. Administration of propranolol and methylscopolamine together, reduced the magnitude of the bradycardia by blocking cardiac efferent mechanisms mediating baroreceptor reflexes, but left a persistent residual fall in heart rate which was independent of baroreflexes; on the other hand when the AVP antagonist was given simultaneously with propranolol and methylscopolamine the bradycardia was completely abolished. Furthermore, infusion of AVP producing plasma levels similar to those seen after A1 lesions, caused a fall in heart rate and cardiac output with only a minor degree of vasoconstriction and no change in mean arterial pressure. An inhibitor of angiotensin converting enzyme had no effect on either heart rate or blood pressure. The rise in blood pressure observed after lesions of the A1 noradrenaline cell region is principally due to activation of the sympatho-adrenal system. The bradycardia is partly reflex due to stimulation of arterial baroreceptors. There is a marked rise in plasma AVP which exerts a minor vasoconstrictor effect but contributes directly and more substantially to the fall in heart rate.
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PMID:The sympatho-adrenal system and vasopressin in cardiovascular responses to A1 lesions. 669 51


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