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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the possible role of arginine vasopressin in maintaining high blood pressure of spontaneously hypertensive rats (SHR), the effect of two arginine vasopressin pressor antagonists on mean arterial pressure and the pressor responsiveness to exogenous arginine vasopressin were studied in conscious, freely moving SHR and in Wistar-Kyoto rats (WKY). Intravenous injections of either d(CH2)5Tyr(Me)arginine vasopressin, 10 micrograms/kg, or dPTyr(Me)arginine vasopressin, 20 micrograms/kg, had no effect on mean arterial pressure or heart rate of normohydrated SHR, although both antagonists almost completely abolished the pressor response to exogenous arginine vasopressin. Furthermore, dPTyr(Me)arginine vasopressin was ineffective in eliciting a depressor response, even after 24 or 48 hours of water deprivation. During converting enzyme inhibition with SQ 20881, mean arterial pressure and heart rate remained unchanged following arginine vasopressin blockade in both normohydrated and fluid-restricted animals. alpha-Adrenergic receptor blockade reduced the blood pressure of normohydrated SHR, from 160 +/- 7 to 81 +/- 8 mm Hg. When dPTyr(Me)arginine vasopressin was given during alpha-adrenergic receptor blockade there was a small, transient fall in mean arterial pressure. The pressor responsiveness to exogenous arginine vasopressin was similar in hypertensive and normotensive rats. These results suggest that arginine vasopressin does not function as an important pressor hormone in conscious SHR.
Hypertension 1986 Jun
PMID:Does vasopressin sustain blood pressure in conscious spontaneously hypertensive rats? 287 62

Fenoldopam mesylate (SK&F 82526-J) is a novel benzazepine derivative. It has selective agonist activity at post-junctional (DA1) vascular dopaminergic receptors, which normally subserve renal artery vasodilation. Previous studies in normal subjects and in patients with hypertension indicate that fenoldopam increases renal blood flow and promotes a sodium diuresis. Drug efficacy was clinically evaluated in eight patients with chronic congestive heart failure (CHF) after a single oral dose of 100 mg of fenoldopam and following 3 days of therapy (100 mg four times daily). Stroke volume index acutely increased from 26 +/- 7 (mean +/- SD) to 30 +/- 4 ml/beat/m2 (p less than 0.05) and left ventricular filling pressure decreased from 26 +/- 13 to 23 +/- 11 mm Hg (p less than 0.05). Systemic vascular resistance decreased from 1513 +/- 159 to 1128 +/- 319 (p less than 0.05). Hemodynamic changes were seen as early as 30 minutes following fenoldopam and returned to control levels by 4 hours. Forearm blood flow, hepatic blood flow, and venous capacitance did not significantly change acutely, but renal blood flow index was significantly reduced (34 +/- 4 to 30 +/- 3 min-1 X 1000, p less than 0.01). Plasma norepinephrine, plasma renin activity, plasma arginine vasopressin, and plasma aldosterone did not significantly change acutely. After 3 days of treatment, 100 mg of fenoldopam again reduced the renal blood flow index (35 +/- 7 to 26 +/- 7 min-1 X 1000, p less than 0.01) and tended to increase plasma renin activity (11.7 +/- 8 to 21.2 +/- 19.4 ng/ml/hr, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic, renal, and neurohumoral effects of a selective oral DA1 receptor agonist (fenoldopam) in patients with congestive heart failure. 289 70

The role of antidiuretic and pressor effects of vasopressin (VP) in deoxycorticosterone acetate (DOCA)-salt hypertension was studied in young and adult Brattleboro rats. The antidiuretic VP action was a necessary prerequisite for the development of severe DOCA-salt hypertension. The insufficient expansion of extracellular fluid volume in DOCA-salt-treated VP-deficient (DI) rats was associated with the attenuation of their hypertensive response, although they had highly increased blood volume and extracellular sodium. Chronic [deamino]-D-arginine vasopressin supplementation that restored volume and distribution of body fluids in DI rats permitted the full development of DOCA-salt hypertension. Blood pressure response to DOCA-salt treatment was always greater in young than in adult Brattleboro rats (even in animals lacking pressor or both VP effects). In animals in which antidiuretic VP effects were present, the pattern of body fluid response to DOCA-salt treatment was also age dependent. There was a tendency to intravascular expansion in young hypertensive rats, whereas an increase of interstitial fluid volume was found in adult animals. The elimination of VP pressor action lowered systemic resistance much more in adult than in young hypertensive rats. We conclude that 1) in adult but not in young rats antidiuretic VP effects are essential for the occurrence of blood pressure response to DOCA-salt treatment, 2) the restoration of body fluids due to antidiuretic VP action enables the development of hypertension in both age groups of DI rats, and 3) pressor VP effects contribute to the maintenance of hypertension, especially in adult animals.
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PMID:Antidiuretic and pressor actions of vasopressin in age-dependent DOCA-salt hypertension. 291 6

Antidiuretic hormone is known to stimulate the renal synthesis of prostaglandins. These autacoids, in turn, modulate the pressure natriuresis phenomenon. Accordingly, the present study was done to test the hypothesis that, in the absence of antidiuretic hormone and antidiuretic hormone-dependent prostaglandin synthesis, the pressure natriuresis response is blunted. Experiments were performed on Brattleboro diabetes insipidus rats (n = 7) and Long Evans control rats (n = 14). A change in perfusion pressure in the Long Evans rats from 89.3 +/- 1.0 to 108.7 +/- 1.1 mm Hg (p less than 0.05) was associated with significant increases in the fractional excretion of sodium (1.1 +/- 0.2 to 2.3 +/- 0.3%) and the urinary prostaglandin excretion (32.6 +/- 6.8 to 56.6 +/- 10.0 pg/min). In contrast, a similar change in perfusion pressure in the diabetes insipidus rat from 88.6 +/- 1.4 to 106.2 +/- 1.5 mm Hg (p less than 0.05) resulted in no significant increases in either sodium or prostaglandin excretions. Treatment of a third group of diabetes insipidus rats (n = 9) with 1-desamino-8-D-arginine vasopressin (1 microgram/day) restored the natriuretic response to increases in renal perfusion pressure. Treated diabetes insipidus and Long Evans control rats had comparable natriuretic responses to increases in renal perfusion pressure. Untreated diabetes insipidus rats, on the other hand, had blunted responses. In summary, the pressure natriuresis response in diabetes insipidus rats is blunted compared with Long Evans control rats. We conclude that antidiuretic hormone is necessary for the complete expression of the pressure natriuresis response.
Hypertension 1989 Apr
PMID:Blunted pressure natriuresis in the Brattleboro diabetes insipidus rat. 292 34

Plasma vasopressin sensitizes the baroreceptor reflex, whereas vasopressin given into the cerebral ventricle overrides the baroreceptor reflex by means of sympathetic stimulation. To test the hypothesis that arginine vasopressin stimulates two different receptor subtypes (V1 and V2) in the central nervous system, we measured the baroreceptor reflex (change in pulse interval vs change in blood pressure) after administering methoxamine (10-300 micrograms/kg i.v.) in conscious rats. Animals were pretreated either with a V1 vasopressin receptor antagonist administered intravenously or intracerebroventricularly, or with a V2 receptor antagonist administered intravenously. The central V1 antagonist caused sensitization of the baroreceptor reflex, whereas the intravenous V2 antagonist attenuated it. The intravenous V1 vasopressin antagonist had no effect on baroreceptor reflex sensitivity. When the experiments were repeated in rats with hereditary diabetes insipidus, neither antagonist influenced the baroreceptor reflex. Volume expansion lowered circulating vasopressin levels and also attenuated the baroreceptor reflex--effects similar to those observed with the intravenous V2 antagonist. We conclude that vasopressin sensitizes the baroreceptor reflex through V2 receptors accessible from the blood and inhibits the reflex through V1 receptors in the brain that cannot be reached from the blood. These observations suggest a direct interaction between hormonal and neuronal vasopressin in cardiovascular control.
Hypertension 1986 Jun
PMID:Differential modulation of the baroreceptor reflex by brain and plasma vasopressin. 294 69

This study compared the haemodynamic and arginine vasopressin responses of patients to fentanyl or sufentanil anaesthesia for coronary artery bypass surgery. Fourteen normotensive patients with normal left ventricular function were studied. Patients were induced with fentanyl (N = 7) 37.5 micrograms X kg-1 or sufentanil (N = 7) 7.5 micrograms X kg-1 by intravenous infusion over three minutes. Clinically important chest wall rigidity, bradycardia and recall of intraoperative events did not occur. All of the fentanyl patients became hypertensive after induction and five required vasodilator therapy since they did not respond to boluses of fentanyl (12.5 micrograms X kg-1). Two of these five patients had S-T depression greater than 1 mm. Five patients in the sufentanil group became hypertensive after induction. Four of these patients responded to additional sufentanil (3.75 micrograms X kg-1) while one required vasodilator therapy for concomitant S-T depression. Sufentanil attenuated the increase of arginine vasopressin during cardiopulmonary bypass. Levels of arginine vasopressin in the fentanyl group were significantly higher than those of the sufentanil group during bypass. Levels of AVP after bypass were higher in the sufentanil group. The incidence of hypertension was similar in both groups. The hypertension was more easily treated with sufentanil but concomitant vasodilators (nitroglycerine) were required in both patient groups. Neither fentanyl in doses up to 128 +/- 8.7 micrograms X kg-1 nor sufentanil in doses up to 23 +/- 1.4 micrograms X kg-1 can be used as sole agents for anaesthesia in adult coronary artery bypass patients with good ventricular function when induction times are three minutes and bolus top-up doses are used.
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PMID:Haemodynamic and plasma vasopressin responses during high-dose fentanyl or sufentanil anaesthesia. 294 80

The gain or sensitivity of reflexes originating in cardiac sensory receptors with vagal afferent pathways is highly dynamic. This modulation is usually attributed to central nervous system or efferent mechanisms. This paper briefly reviews evidence that modulation of reflexes originating in the heart can also occur at the sensory or afferent level. Five examples are cited: calcium antagonists, cardiac glycosides, arginine vasopressin, atrial natriuretic peptides, and changes in dietary sodium. These examples emphasize the role of ionic and humoral factors in regulation of cardiac vagal afferent function. This concept of sensory modulation of cardiac vagal afferents has implications for cardiovascular pharmacology and for pathophysiological states such as heart failure and hypertension.
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PMID:Sensitization of cardiac vagal afferent reflexes at the sensory receptor level: an overview. 294 40

Our previous studies have demonstrated that LY171555 (quinpirole), a specific dopamine (DA) D2-receptor agonist, has a pressor effect in the conscious rat which is accompanied by increased sympathetic outflow and arginine vasopressin release. To test the hypothesis that LY171555 inhibits in vivo release of DA and its metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), from central dopaminergic neurons of the conscious, freely moving rat by activation of presynaptic DA receptors in the central nervous system and that this mechanism may be altered in the desoxycorticosterone acetate (DOCA)/NaCl model of hypertension, we used the in vivo push-pull perfusion method to study the effect of LY171555 on central DA release in normotensive and DOCA/NaCl-hypertensive rats. Levels of the DOPAC and HVA were measured in striatal perfusates by HPLC before and after administration of LY171555 (1 mg/kg, i.v.) of conscious, unrestrained 4-week DOCA/NaCl hypertensive and uninephrectomized H2O control rats. There were no significant differences in basal striatal HVA (80 +/- 12 vs 89 +/- 11 pg/min; DOCA/NaCl vs control) or DOPAC levels (37 +/- 5 vs 49 +/- 17 pg/min; DOCA/NaCl vs control) during the entire 240-min collection period. LY171555 significantly reduced HVA and DOPAC levels in perfused striatum in both normotensive control and DOCA/NaCl-hypertensive rats. The LY171555-induced suppression in HVA levels was significantly greater in DOCA/NaCl rats (delta = 60.7 +/- 3.6%) than in H2O controls (delta = 49.0 +/- 3.5%, P less than 0.05). Pretreatment with metoclopramide (10 mg/kg, i.v.), a specific central and peripheral DA D2-receptor antagonist, completely blocked the suppressive effects of LY171555 on HVA and DOPAC levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhanced response to the inhibitory action of LY171555, a dopamine D2-agonist, on in vivo striatal dopamine release in DOCA/NaCl-hypertensive rats. 294 97

Studies done in vitro have demonstrated that atrial natriuretic peptide (ANP) antagonizes angiotensin II-mediated contraction of vascular smooth muscle. The present studies were designed to examine the in vivo actions of ANP in acute angiotensin II-mediated hypertension. The cardiovascular, renal, and hormonal effects of intravenous ANP were evaluated in anesthetized normotensive (n = 6) and hypertensive (n = 6) dogs. In both groups, ANP (3.0 micrograms/kg bolus, 0.3 micrograms/kg/min continuous infusion) reduced arterial pressure and cardiac output without changing systemic vascular resistance. ANP specifically reduced renal vascular resistance and increased sodium excretion. The natriuresis observed was greater in hypertensive than in normotensive dogs. This occurred without a significant change in glomerular filtration rate or aldosterone. The ANP-mediated reduction in arterial pressure was associated with an increase in circulating arginine vasopressin and catecholamines but not in renin. These studies demonstrate that ANP-mediated hypotension results from a reduction in cardiac output without changing systemic vascular resistance, ANP acts as a specific renal vasodilator, ANP-mediated natriuresis can occur without alteration in glomerular filtration rate or aldosterone, and ANP specifically inhibits the release of renin without inhibiting the release of other circulating vasoconstrictors.
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PMID:Cardiovascular, renal, and endocrine response to atrial natriuretic peptide in angiotensin II mediated hypertension. 294 86

The hypothesis that the vasoconstrictor action of vasopressin may contribute to the development of hypertension in spontaneously hypertensive rats (SHR) was tested by chronic infusion of a specific antagonist of the vascular effects of vasopressin. From 4 to 13 weeks of age, SHR and Wistar-Kyoto rats (WKY) received subcutaneously either isotonic saline or the vasopressin pressor antagonist, d(CH2)5Tyr(Me)arginine vasopressin by osmopump. Systolic blood pressure was measured by tail cuff from 5 to 11 weeks of age. In SHR, the vasopressin analogue did not alter the rate or magnitude of increase in systolic blood pressure. In WKY, systolic blood pressure in the vasopressin analogue group was slightly reduced compared with the saline infusion values until 10 weeks of age (F1, 10 = 10.18, p = 0.008). At 12 to 14 weeks of age, all animals were prepared with indwelling arterial and venous catheters. Resting mean arterial pressure was not altered significantly by the vasopressin analogue infusion in either strain, but the response to an acute vasopressin infusion of 5, 15, or 50 ng/kg body weight was markedly attenuated by the analogue treatment, indicating that plasma levels of the vasopressin analogue were sufficient to block pressor effects of endogenous vasopressin. A bolus injection of the angiotensin II converting enzyme inhibitor teprotide (SQ 20881) resulted in a decrease in mean arterial pressure (p less than 0.05) that was comparable in all groups, and serum renin concentration was not elevated in the vasopressin analogue-treated rat.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1987 Apr
PMID:Evidence against a pressor role for vasopressin in spontaneous hypertension. 295 26


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