BLOOD-PRESSURE DEPENDENCY ON VASOPRESSIN AND ANGIOTENSIN-II IN PRAZOSIN-TREATED CONSCIOUS NORMOTENSIVE RATS

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  • 1 January 1983
    • journal article
    • research article
    • Vol. 225  (2) , 442-446
Abstract
The role of the sympathetic nervous system, angiotensin II and vasopressin in limiting the hypotensive effect of prazosin (0.25 mg i.v.) was investigated in conscious normotensive rats. Within 45 min, mean blood pressure fell from 120 .+-. 1 to 98 .+-. 1 mm Hg (mean .+-. S.E.M [standard error of the mean], P < .001) while pulse rate rose from 463 .+-. 9 to 500 .+-. 9 beats/min (P < .01). The blood pressure response to prazosin tended to be most pronounced in the rats with the smallest increase in heart rate (r = 0.58, P < .001). Plasma norepinephrine and epinephrine levels were higher in prazosin-treated rats than in the controls (P < .001). In the animals receiving prazosin, plasma renin activity was 4 times (P < .001) and plasma vasopressin 7 times (P < .01) higher than in the controls. Blockade of angiotensin II with saralasin (10 .mu.g/min) further decreased blood pressure of the prazosin-treated rats by 22 .+-. 4 mm Hg (P < .001). dPVDAVP (25 .mu.g), a vasopressin antagonist, had no effect. Prazosin decreased the pressor response to methoxamine (10 .mu.g) by 80% (P < .001) but not to angiotensin II (60 ng). Prazosin enhanced the reflex bradycardia induced by angiotensin II (P < .001). Both the sympathetic and the renin angiotensin system are evidently markedly stimulated by prazosin; they both appear to limit its acute hypotensive action. Although plasma vasopressin is also increased, its pressor action is effectively buffered, probably due to enhanced baroreflex sensitivity.