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

Electrical stimulation of afferent renal nerves and activation of renal mechanoreceptors increase plasma vasopressin concentrations. In the present study, the effect of renal chemoreceptor activation on plasma vasopressin concentration was investigated in anesthetized rabbits. Renal chemoreceptors were activated with intrarenal infusions of bradykinin. With intrarenal infusion of bradykinin at 136 ng/min, plasma vasopressin concentration increased from 4.5 +/- 1.5 to 26.8 +/- 14.2 pg/ml at 5 minutes (p less than 0.01), whereas with infusion at 1,360 ng/min, plasma vasopressin increased from 5.9 +/- 2.0 to 54.4 +/- 16.4 pg/ml at 5 minutes (p less than 0.01). There was no significant change in plasma vasopressin during intravenous infusion of bradykinin at 136 ng/min. Infusion at 1,360 ng/min increased plasma vasopressin from 2.7 +/- 0.5 to 14.8 +/- 6.4 pg/ml (p less than 0.01), but this increase was significantly less than that produced by intrarenal infusion of the same dose of bradykinin. Similar effects on plasma vasopressin were observed during paired intrarenal and intravenous infusions of bradykinin at 136 ng/min. Renal denervation markedly reduced the vasopressin responses to intrarenal infusion of bradykinin at 136 ng/min (2.8 +/- 0.5 to 4.0 +/- 0.7 pg/ml, p less than 0.01) and 1,360 ng/min (3.2 +/- 0.7 to 7.8 +/- 1.8 pg/ml, p less than 0.05). These results indicate that bradykinin stimulates vasopressin release by an intrarenal action and suggest that this action is mediated by afferent renal nerves.
Hypertension 1992 Jun
PMID:Effect of intrarenal bradykinin infusion on vasopressin release in rabbits. 159 84

The hemodynamic responses and the role of renal nerves in the physiopathogenesis of acute (45 min) aortic coarctation hypertension were studied in conscious rats. The hemodynamic responses elicited by aortic constriction in intact and bilaterally nephrectomized rats were analyzed by means of miniaturized pulsed-Doppler flow probes. Anephric rats presented a smaller increase in mean carotid pressure (MCP) and calculated aortic resistance during aortic coarctation than did intact animals. Reflex bradycardia throughout the experiment did not differ significantly between the two groups. The pressor response following aortic coarctation in untreated renal-denervated rats was similar to that found in intact subjects. Renal-denervated rats previously treated with V1-vascular arginine vasopressin antagonist [d(CH2)5Tyr(Me)AVP] showed the same hypertensive response as control renal-denervated rats. Previous treatment of renal-denervated rats with saralasin (an angiotensin II antagonist) produced a significant reduction in the hypertensive response throughout the experiment when compared to untreated renal-denervated rats. Similarly, rats treated with the vasopressin antagonist plus saralasin showed a blunted hypertensive response following aortic coarctation. The results for rats previously treated with vasopressin antagonist plus saralasin did not differ from those obtained with saralasin alone. Overall, the results of aortic coarctation hypertension obtained in the present study indicate that: 1) Anephric rats showed a blunted hypertensive response due to the lack of neuro-humoral release of vasopressor substances (e.g. angiotensin II and vasopressin) triggered by the kidneys, when only the mechanical factor of constriction was present; 2) The lack of afferent feedback from the kidneys in renal-denervated rats for vasopressin release from the central nervous system allowed angiotensin II to play the major physiopathological role associated with the mechanical factor in the hypertensive response.
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PMID:Mechanical and neuro-humoral factors in acute aortic coarctation hypertension. 160 37

The contribution of the sympathetic nervous system and vasopressin to the maintenance of arterial pressure was investigated in high sodium-fed rats 4 weeks after the induction of one-kidney, figure-8 renal wrap hypertension. Arterial pressure was significantly greater in renal-wrapped rats than in sham-operated animals. The contribution of the sympathetic nervous system was assessed functionally by measuring the arterial pressure response to ganglionic blockade and estimating the apparent rate of release of norepinephrine. The contribution of vasopressin was assessed by administration of the vascular antagonist d(CH2)5Tyr(Me)-AVP. Whole-animal vascular responsiveness and cardiac baroreceptor reflex sensitivity were determined by graded intravenous bolus injections of angiotensin II, vasopressin, and phenylephrine. Hypertensive rats demonstrated an exaggerated reduction in arterial pressure to autonomic blockade before and after blockade of vascular vasopressin receptors. There was a significant 27% increase in the apparent rate of release of norepinephrine into the plasma. Administration of d(CH2)5Tyr(Me)-AVP did not affect arterial pressure when given alone. However, after ganglionic blockade, inhibition of the vasopressin system elicited similar falls in blood pressure in both normotensive and hypertensive rats. Arterial pressure dose-response effects of phenylephrine, angiotensin II, and vasopressin were similar between renal-wrapped and sham-operated animals; however, cardiac baroreceptor reflex sensitivity was suppressed in the hypertensive rats. These studies indicate that the maintenance of arterial pressure in chronic, high sodium renal-wrap hypertension is associated with an augmented sympathetic nervous system function.
Hypertension 1992 Jul
PMID:Sympathetic nervous system in high sodium one-kidney, figure-8 renal hypertension. 161 57

Several recent reports have suggested that pressor hormones may be released during and after carotid endarterectomy and that release of these factors may be associated with postoperative hypertension and other postoperative morbidity. We measured vasopressin, adrenocorticotropic hormone, and cortisol in jugular venous blood during carotid endarterectomy under general anesthesia in 43 patients with routine carotid shunting. Jugular venous vasopressin increased significantly after the second period of carotid occlusion for shunt removal and remained increased at closure. Vasopressin did not change during the initial carotid occlusion for shunt placement or during the endarterectomy itself, and neither ACTH nor cortisol changed at any sample time. Greater resting vasopressin and cortisol and larger responses of vasopressin were observed in patients receiving phenylephrine to correct intraoperative hypotension. There were no correlations between postoperative hypertension or postoperative complications and intraoperative hormone values. These results suggest (1) basal intraoperative vasopressin values reflect the blood volume of the patient, (2) increased vasopressin was not related to postoperative morbidity, and (3) intraoperative increases in pressor hormones are most likely physiologic responses to specific stimuli such as hypovolemia or hypotension rather than pathologic phenomena. We speculate that the increase of vasopressin after the second carotid occlusion and reperfusion of the brain may be due to the action of humoral factors released into the carotid circulation from the endarterectomy site.
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PMID:Jugular venous vasopressin increases during carotid endarterectomy after cerebral reperfusion. 161 7

The mechanisms of anti-hypertensive effect of diuretics remain unknown. The purpose of this study was to test the hypothesis that long-term treatment with chlorthalidone decreases the responsiveness of resistance vessels to neurohormones. The study was performed in deoxycorticosterone acetate (DOCA)-salt hypertensive rats with and without treatment with chlorthalidone (Chlor. 8 mg/day, for 20 days). Resting mean arterial pressure in freely moving state was significantly reduced in DOCA-salt-Chlor rats when compared to DOCA-salt rats (116 +/- 3 vs 147 +/- 7 mmHg, respectively). Chlorthalidone treatment reduced the high plasma sodium content observed in DOCA-salt rats to the same levels observed in normotensive control groups. Results obtained in isolated perfused mesenteric arteries showed: a) the increase in perfusion pressure elicited by norepinephrine (NE), serotonin (SE) and vasopressin (VP) was significantly greater in DOCA-salt than in DOCA-salt + Chlor rats or control normotensive rats; b) the endothelium removal increased the pressor responses to NE, SE and VP in a similar way in all groups. These data provide evidence that long-term chlorthalidone treatment reduces vascular hyperresponsiveness to these neurohormones. In addition, these results indicate that this reduction in vascular hyperresponsiveness, associated with a decrease in extracellular sodium level, could be a possible mechanism by which the diuretics reduce the high blood pressure.
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PMID:Chlorthalidone reduces vascular hyperresponsiveness in DOCA-salt hypertensive rats. 162 12

The influence of chronic saline drinking and/or DOCA-salt treatment on plasma renin activity and renal renin concentration was studied in vasopressin-deficient homozygous (DI) Brattleboro rats and their vasopressin-secreting heterozygous (non-DI) littermates. The activity of renin-angiotensin system (RAS) can be suppressed even in the absence of vasopressin under the conditions of a sufficiently high salt intake that is achieved in DI rats by consumption of 0.6% saline instead of water. An almost complete RAS suppression in both plasma and kidney was observed in young animals in which high salt intake induced not only blood volume expansion but also blood pressure elevation, i.e. in mildly hypertensive unilaterally nephrectomized saline drinking DI rats as well as in moderately hypertensive DOCA-salt treated DI rats and in non-DI rats with a severe DOCA-salt hypertension. Our results indicate that intravascular expansion and blood pressure changes are important factors for the modulation of plasma and renal renin activity even in the absence of vasopressin.
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PMID:The influence of high salt intake and/or chronic blood volume expansion on renin-angiotensin system in Brattleboro rats. 163 41

Previous studies have shown that inhibition of the lipoxygenase pathway of arachidonic acid metabolism can prevent the development of elevated blood pressure in renin-dependent models of hypertension. Agents that inhibit the lipoxygenase pathway such as phenidone and the flavonoid baicalein can selectively attenuate contractile responses to angiotensin II in vivo as well as in isolated vascular tissue. In the present study, the effects of lipoxygenase inhibitors on pressor-induced changes in cytosolic calcium were examined in cultured rat vascular smooth muscle cells using the fluorescent dye fura-2. Two structurally unrelated lipoxygenase inhibitors, baicalein and 5,8,11-eicosatriynoic acid, attenuated angiotensin II-stimulated increases in cytosolic calcium in both normal and calcium-poor buffer. The addition of 5-, 12-, or 15(S)-hydroxyeicosatetraenoic acid alone to the cells had no acute effect on intracellular calcium concentration. However, the addition of 12(S)-hydroxyeicosatetraenoic acid but not 5- or 15(S)-hydroxyeicosatetraenoic acid restored the initial calcium response to angiotensin II in vascular smooth muscle cells pretreated with both inhibitors; 5,8,11-eicosatriynoic acid also reduced [Arg8]-vasopressin and endothelin-stimulated increases in intracellular calcium. The attenuation of vasopressor-induced calcium transients by agents that inhibit lipoxygenase may explain their observed hypotensive effects in vivo. Moreover, lipoxygenase products, in particular 12(S)-hydroxyeicosatetraenoic acid, may act as mediators for the intracellular actions of angiotensin II and possibly other pressor hormones in vascular tissue by regulation of intracellular calcium metabolism.
Hypertension 1992 Aug
PMID:12-Lipoxygenase products modulate calcium signals in vascular smooth muscle cells. 163 55

To investigate the time course of the effects of alcohol on blood pressure, we studied the response of ambulatory blood pressure, neurohumoral variables, and hemodynamics to a single moderate dose of alcohol in hypertensive patients. Sixteen Japanese men (22-70 years old) with essential hypertension who were habitual drinkers were examined under standardized conditions. On the alcohol intake day, they ingested 1 ml/kg ethanol (vodka) at dinner, and on the control day they consumed a nonalcoholic beverage. The order of the two periods was randomized. Mean ambulatory blood pressure was lower in the alcohol intake period than in the control period (125 +/- 3/74 +/- 2 versus 132 +/- 4/78 +/- 2 mm Hg, p less than 0.05), and the significant depressor effect of alcohol lasted for up to 8 hours after drinking. Blood pressure on the next day did not differ with or without alcohol intake. The acute hypotensive effect of alcohol was associated with an increase in heart rate and cardiac output and with a decrease in systemic vascular resistance as determined by echocardiography. Plasma catecholamine levels and renin activity rose significantly at 2 hours after dinner, whereas vasopressin and potassium levels fell on the alcohol day. Blood glucose and serum insulin levels were comparable between the two periods. Three patients with marked alcohol-induced flush had greater hypotensive and tachycardiac responses than those who did not show an alcohol-induced flush. The change in mean blood pressure induced by alcohol was negatively correlated with age, the baseline blood pressure, and the change in plasma norepinephrine. These results indicate that the major effect of acute alcohol intake is to lower blood pressure through systemic vasodilatation in hypertensive subjects. Ambulatory blood pressure monitoring may be useful for assessing blood pressure in habitual drinkers.
Hypertension 1992 Aug
PMID:Acute depressor effect of alcohol in patients with essential hypertension. 163 64

Behavioral stress and high dietary salt have been reported to increase blood pressure additively in non-human primates. This study was designed to replicate this phenomenon and to assess neuroendocrine correlates and responses to two commonly used antihypertensives, a beta-adrenoceptor blocker and a thiazide diuretic. High-salt intake (240 mmol sodium per day) and stress were administered for 9 weeks in adult baboons. Oral atenolol hydrochloride (50 mg, twice daily) or hydrochlorothiazide (25 mg/day) was administered for 2 weeks each. In all four baboons, salt loading and stress increased systolic blood pressure (SBP) chronically by 14 mmHg, with increases in water intake, urine osmolality and excretion of sodium, decreases in levels of serum sodium, plasma renin activity and plasma vasopressin and no changes in urinary excretion of norepinephrine or epinephrine. Neither drug decreased SBP during ongoing high salt and stress. The results confirm the additive chronic effects of high-dietary salt intake and behavioral stress on blood pressure in non-human primates. The hypertension in this model is resistant to two antihypertensive drugs commonly used clinically.
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PMID:Stress and sodium hypertension in baboons: neuroendocrine and pharmacotherapeutic assessments. 165 40

A group of consecutive 180 veteran patients with mild to moderate essential hypertension were chosen to participate in clinical antihypertensive trial for the purpose of defining the role of converting enzyme inhibitors and renin-angiotensin-aldosterone system in the management of mild to moderate hypertension patients. After a two-week placebo period, these patients were randomly assigned to regimens of converting enzyme inhibitors (enalapril or captopril with or without diuretics) or conventional therapy (diuretics with or without traditional vasodilators with or without beta-blockers). Each patient was regularly followed up every two weeks and doses were added until the diastolic blood pressure was equal to or lower than 90 mmHg. After 1 year of follow-up, only 162 patients completed the study. All high blood pressure was significantly reduced by these three regimens, but no significant difference of blood pressure control was noted. The mean left ventricular ejection fraction increased from 55.9 +/- 6.2 to 57.5 +/- 5.3% in captopril group (P less than 0.05, n = 59) and from 54.8 +/- 6.8 to 57.2 +/- 5.8% enalapril group (P less than 0.01, n = 53), in contrast to the insignificant change in control group (n = 50) (56.5 +/- 7.7 to 56.6 +/- 5.9%). The exercise duration also significantly increased only in converting enzyme inhibitors group (P less than 0.01). Furthermore, the plasma aldosterone level was significantly reduced by converting enzyme inhibitors therapy, whereas conventional therapy had no beneficial effect (P less than 0.01). Furthermore, the plasma aldosterone level was significantly reduced by converting enzyme inhibitors therapy, whereas conventional therapy had no beneficial effect (P less than 0.001). Concomitantly, antidiuretic hormone and plasma norepinephrine levels were also significantly reduced by converting enzyme inhibitors. In addition, converting enzyme inhibitors had a favorable trend to affect the metabolism of lipid in contrast to the conventional therapy. These results show that a first-step treatment of hypertension with converting enzyme inhibitors permits better left ventricular function and improves exercise tolerance by way of renin-angiotensin-aldosterone system inhibition. Thus, converting enzyme inhibitors might be suggested as the first step regimen in the treatment of hypertension.
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PMID:Comparisons of long-term effects between converting enzyme inhibitors and conventional therapy in treating mild to moderate hypertension. 165 34


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