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)

Ten patients with advanced congestive heart failure were treated with an arginine vasopressin V1 antagonist during hemodynamic monitoring to determine the contribution of vasopressin to vasoconstriction in this disorder. The vasopressin antagonist caused a decrease in systemic vascular resistance in the three patients whose plasma vasopressin was greater than 4.0 pg/ml (average for the group was 2.4 +/- 0.6). Plasma vasopressin concentration correlated with the percent decrease of systemic vascular resistance (r = 0.70, p less than 0.025), serum sodium (r = 0.72, p less than 0.02) and serum creatinine (r = 0.85, p less than 0.005). To compare the relative roles of vasopressin, the renin-angiotensin system and the sympathetic nervous system, these patients also received captopril and phentolamine. Captopril decreased systemic vascular resistance by 20% (p less than 0.05), mostly in patients with high plasma renin activity. Levels of plasma renin activity ranged between 1 and 46 ng/ml per h (average 14.7 +/- 5.7) and correlated with serum sodium (r = 0.77, p less than 0.025), serum creatinine (r = 0.73, p less than 0.025) and right atrial pressure (r = 0.67, p less than 0.05). Phentolamine decreased systemic vascular resistance in all patients (average 34%, p less than 0.01), but the decrease did not correlate with the pretreatment norepinephrine concentration. Norepinephrine levels were elevated in all patients (694 +/- 110 pg/ml) and correlated with baseline stroke volume index (r = 0.75, p less than 0.025) and plasma renin activity (r = 0.67, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contribution of vasopressin to vasoconstriction in patients with congestive heart failure: comparison with the renin-angiotensin system and the sympathetic nervous system. 351 28

In the past, hemodynamic factors, in congestive heart failure were considered as being of major importance in the production of the major symptoms and signs of the disease: peripheral (increased oxygen extraction, flow redistribution) or central (Starling's law, myocardial contractility). More recently, excessive hormonal compensation has been felt to be more important such as: The renine-angiotensin-aldosterone axis, Circulating catecholamines, Arginin-vasopressin. These hormones are responsible for water and sodium retention, tachycardia and increase in peripheral resistance. Newer agents such as Captopril are effective in blocking the action of these endocrine factors.
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PMID:[Treatment of congestive heart failure: new concepts]. 352 15

In the pithed Wistar rats Captopril (2 mg/kg) decreased the mean arterial pressure (MAP) 21%. Further injection of a specific antagonist decreased the vasoconstrictor action of vasopressin (aAVP, 10 micrograms/kg) an additional 6%. Reversal in the order of drug administration did not change these percentages. The osmotic stimulus evoked by the infusion of hypertonic saline (ClNa 9%, 0.018 ml/min, 2 hr) significantly increased MAP, this increase being almost totally reversed by the aAVP (10 micrograms/kg). These findings suggest a greater role of the renin-angiotensin system than of the vasopressin (AVP) in the maintenance of MAP in the pithed rat; AVP, moreover, can be released by means of an osmotic stimulus.
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PMID:Blood pressure control in pithed rat. 353 Aug 77

We have previously demonstrated that chronic intracerebroventricular (ICV) administration of captopril attenuates the development of hypertension in young SHR in association with a depression in whole animal reactivity to vasoactive agents and an increased baroreflex sensitivity. In the present study we analyzed vascular reactivity in perfused kidneys from SHR treated with captopril or vehicle to determine whether the depression in reactivity was due to changes in baroreflex activity or an effect on the vasculature. Captopril (1.25 micrograms/hr) was infused (osmotic mini pumps) for 4 weeks. Vascular reactivity to norepinephrine, angiotensin and vasopressin was assessed in isolated kidneys perfused with an artificial medium at constant flow. SHR treated with ICV captopril showed a significantly lower arterial pressure and basal renal vascular resistance than SHR treated with ICV vehicle or IV captopril. In addition, these rats showed decreased vascular reactivity to all vasoactive agents tested as signified by a shift in the dose-response curves to the right with an increase in threshold (ED16) and ED50. Kidneys from WKY treated with ICV captopril also showed a decrease in vascular reactivity in comparison to WKY treated with ICV vehicle. Our data suggest that captopril, through a central action, attenuates the development of hypertension by decreasing vascular reactivity to vasoconstrictors.
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PMID:Alterations in renal vascular reactivity induced by chronic central administration of captopril in the spontaneously hypertensive rat. 353 26

The separate role of mineralocorticoid and glucocorticoid hormone action in maintaining arterial pressure was studied in normotensive rats. Four groups were prepared: adrenalectomized (ADX) rats given 6 micrograms aldosterone/24 h (ALDO; n = 9) or 10 micrograms dexamethasone/24 h (DEX; n = 9) by intraperitoneal Alzet pumps, shamoperated controls (control; n = 10) and ADX rats with no hormone replacement (ADX; n = 9). All groups were given 1% NaCl + 2.5% glucose drinking solution. Measurements of plasma corticosterone and aldosterone and urinary aldosterone excretion confirmed the adequacy of the experimental groups. Forty-eight hours after ADX or sham, base-line intra-arterial mean arterial pressure (MAP) in conscious undisturbed rats was similar in the four groups. Captopril (1 mg/kg iv) produced a similar reduction in MAP in ALDO (-11 +/- 2 mmHg) and DEX (-12 +/- 1 mmHg) groups, despite a lower plasma renin activity (PRA) in ALDO (2.0 +/- 0.7 and 6.0 +/- 1.5 ng X ml-1 X h-1, respectively; P less than 0.05). dP (Me)TyrAVP (50 micrograms/kg iv) caused a greater decrease in MAP in ALDO (-15 +/- 3 mmHg) than in DEX (-8 +/- 1 mmHg; P less than 0.05). Combined blockade with both antagonists resulted in a greater MAP reduction in ALDO (-29 +/- 4 mmHg) than in DEX (-15 +/- 4 mmHg; P less than 0.05). These results indicate that glucocorticoid hormone action maintains arterial pressure in ADX rats by mechanisms similar to normal rats and largely independent of the renin-angiotensin system and vasopressin. In contrast, mineralocorticoid replacement alone in ADX rats requires increased participation of both peptide systems for maintenance of arterial pressure.
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PMID:Role of mineralocorticoids and glucocorticoids in blood pressure regulation in normotensive rats. 353 7

The role of the sympathetic nervous system, angiotensin II (ANG II), and arginine vasopressin (AVP) in maintaining blood pressure (BP) during endotoxic shock was investigated in 117 conscious male Wistar rats. After intravenous injection of 2 mg Escherichia coli endotoxin, mean BP fell within 5 min by approximately 50 mmHg and rose again to approach base-line levels within 90 min. At that time, plasma renin activity, plasma norepinephrine (NE), and vasopressin levels of the endotoxin-treated animals were, respectively, 12-, 10-, and 54-fold (P less than 0.001) higher than those of the controls. The BP effect of either prazosin (0.125 mg iv), captopril (2.5 mg iv), or d(CH2)5Tyr(Me)AVP (5 micrograms iv), a specific antagonist of the vascular effect of AVP, was evaluated over a 30-min observation period starting 90 min after administration of endotoxin or its vehicle. Captopril reduced mean BP from 116 +/- 1.8 to a low of 109 +/- 2.1 (SE) mmHg (P less than 0.05, n = 8) only in rats pretreated with endotoxin, whereas the vasopressin antagonist had no depressor effect even during endotoxemia. The BP drop induced by prazosin in rats exposed to endotoxin (-21 +/- 3.3 mmHg, n = 6) did not significantly differ from that observed in control rats (-14 +/- 3.4 mmHg, n = 6). A dose-response curve to NE, ANG II, and lysine vasopressin was also performed. In endotoxin-treated rats the mean BP response to all agonists was markedly suppressed (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Angiotensin II, vasopressin, and sympathetic activity in conscious rats with endotoxemia. 390 75

Osmoregulation during pregnancy was compared in Brattleboro rats completely lacking vasopressin [homozygous (DI)], those with partial deficiency [heterozygous (HZ)], and control Long-Evans (LE) animals. Plasma osmolality (Posmol) was decreased 10-16 mosmol/kg near term in each group, whereas urine osmolality (Uosmol) was similar to that of virgin controls. This was accompanied by significant increments in water turnover similar in HZ and LE and massive in the gravid DI. Chronic vasopressin treatment increased Uosmol less in pregnant DI compared with virgins (P less than 0.001), and urinary prostaglandin E2 was increased in all gravid groups. Captopril per os failed to implicate the renin-angiotensin system in the altered water ingestive behavior of pregnancy. Basal arginine vasopressin pressure (PAVP) was similar in gravid and virgin HZ and LE, whereas the osmotic threshold for AVP secretion was lower in both pregnant groups. Increasing Posmol by dehydration or hypertonic saline led to similar increments in plasma AVP (PAVP) in pregnant and nongravid rats of each group, but sensitivity of the system delta P AVP/delta P osmol was significantly lower in HZ, a difference compatible with the decreased pituitary AVP content in the HZ strain. Data are consistent with decreases in the osmotic thresholds for AVP release (in HZ and LE) and thirst (in DI) and a need for increased AVP secretion during pregnancy.
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PMID:Osmoregulation and vasopressin secretion during pregnancy in Brattleboro rats. 397 Jan 84

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

Captopril significantly diminished the basal diastolic blood pressure and the vasopressor response to electrical stimulation of the thoracic-lumbar spinal cord in pithed normotensive rats. The reduction of the hypertensive response to electrical stimulation was more pronounced after bilateral adrenalectomy. Captopril also diminished the vasopressor response to intravenously administered (-)-noradrenaline. Pretreatment of the animals with indomethacin had no effect on the vasopressor response to electrical stimulation and did not affect the sympathoinhibition of captopril. After bilateral nephrectomy, 18-24 h previously, the basal diastolic blood pressure and the vasopressor response to electrical stimulation were reduced and captopril had no additional inhibitory effect on these parameters. In indomethacin-pretreated animals with intact kidneys, restoration of the basal diastolic blood pressure with angiotensin II (AII) completely abolished the sympathodepressive effect of captopril. When the reduction in basal diastolic blood pressure with captopril was prevented by vasopressin, converting enzyme inhibition had no depressive effect on the hypertensive response to intravenously administered (-)-noradrenaline and did not influence sympathetic neurotransmission in animals with intact adrenals. However, a small, but significant reduction of the hypertensive response to electrical stimulation by captopril was still detectable in bilaterally adrenalectomized rats. The results suggest that endogenous AII facilitates sympathetic neurotransmission in vascular smooth muscle of pithed normotensive rats. However, the modulatory action of endogenous AII largely results from an effect on basal arteriolar smooth muscle tone and should, therefore, be considered as non-specific facilitation. Genuine prejunctional facilitation of the sympathetic neurotransmission in vascular smooth muscle can only be observed after bilateral adrenalectomy but this effect of endogenous AII appears of minor significance, at least in pithed normotensive rats.
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PMID:Effect of captopril on sympathetic neurotransmission in pithed normotensive rats. 630 8

We have investigated the relative importance of angiotensin and vasopressin in the regulation of arterial pressure following permanent interruption of supraspinal sympathetic influences. To accomplish this aim, the spinal cord of 12 dogs was transected just above the intervertebral foramen of C-6; several days later, we gave first a potent blocker of the vasculotropic actions of vasopressin and 40 min later captopril. The same experiment was performed in other dogs with the drug order reversed. Mean arterial pressure and heart rate were recorded continuously and blood samples were taken to measure plasma renin activity and plasma catecholamines. All studies were carried out at three levels of hydration: normal, after 36 h water deprivation and following an overnight infusion of 0.9% saline. Conscious dogs with complete surgical sympathectomy by spinal cord section had normal mean arterial pressure, heart rate and plasma renin activity but undetectable levels of catecholamines. Captopril produced significant falls in mean arterial pressure that were greatest in water deprivation and least in volume loading, whether the drug was given before or after treatment with the vasopressin antagonist. On the other hand, the vasopressin antagonist modified mean arterial pressure only in the water deprived state. In spinal dogs the renin angiotensin system assumes a primary role in maintaining normal mean arterial pressure at various extremes of body fluid volumes. Vasopressin plays a role only after removal of the two dominant systems.
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PMID:Hierarchy of blood pressure control mechanisms after spinal sympathectomy. 640 Jan 21


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