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J Cardiovasc Pharmacol ; 6(1): 201-5, 1984.
Article in English | MEDLINE | ID: mdl-6199605

ABSTRACT

We previously have demonstrated that the sympathetic nervous system is activated proportionately to the degree of vasodepression induced in hypertensive patients. In the present study, the role of the renin-angiotensin system in modulating the vasodepressor response to sodium nitroprusside was examined. Nine hospitalized hypertensive patients receiving a diuretic were given serially incremental doses of sodium nitroprusside over a dose range of 0.05-4.8 micrograms/kg/min with each dose being infused for 10 min. Mean arterial pressure (MAP), heart rate (HR), plasma renin activity (PRA), and plasma norepinephrine (NE) concentration were measured prior to and during each dose level of sodium nitroprusside. Stepwise increments in PRA were seen in each patient as the dose of sodium nitroprusside was increased. The increase in PRA was proportional to the increase in plasma NE concentration and to the decrease in MAP in each patient. However, considerable intersubject variation was seen in these relationships. When examined by multiple linear stepwise regression analysis, the degree of vasodepression was found to be dependent on the baseline blood pressure and baroreflex sensitivity (r = 0.97). However, increment in PRA was not an independent determinant of the vasodepressor response. Thus, the renin angiotensin system may not be a significant component of the acute homeostatic response to vasodepression in these patients.


Subject(s)
Ferricyanides/therapeutic use , Hypertension/drug therapy , Nitroprusside/therapeutic use , Renin-Angiotensin System/drug effects , Blood Pressure/drug effects , Depression, Chemical , Heart Rate/drug effects , Homeostasis , Humans , Hydrochlorothiazide/therapeutic use , Male , Middle Aged , Norepinephrine/blood , Pressoreceptors/drug effects
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