Hypertension, Vol 5, 312-320, Copyright © 1983 by American Heart Association
C Richer, MP Doussau and JF Giudicelli
The present study compares the effects of short-term treatments with
captopril and enalapril, administered in equipotent antihypertensive doses,
on the regional vascular resistances and on the regional vascular
responsiveness to vasopressor agents of adult spontaneously hypertensive
rats (SHRs). Three groups of animals were treated by gavage with captopril
(100 mg/kg), enalapril (25 mg/kg), or distilled water for 8 days. Arterial
blood pressure (BP), heart rate (HR), plasma renin concentration (PRC), and
plasma converting-enzyme activity (CEA) were measured. Cardiac index (CI),
total peripheral resistance (PR), and organ flow distribution were
determined using microspheres. Renal and mesenteric vascular responsiveness
to vasopressor agents was evaluated by continuous measurement of renal and
mesenteric blood flows with miniaturized pulsed Doppler flow probes. Data
showed that in the anesthetized SHR the two drugs induced similar
reductions in BP, PR, and HR, without affecting CI. They simultaneously
produced a strong converting-enzyme inhibition as evidenced by the
suppression of angiotensin I effects accompanied by a potentiation of
angiotensin II responses, a reduction in CEA, and an increase in PRC. Organ
flows were similarly and homogeneously increased, especially in the
kidneys, in both treated groups. Norepinephrine (NE) vasoconstrictor
responses were abolished in the mesenteric vascular bed by both drugs, but
in the renal, NE responses although completely abolished by captopril were
only partially reduced by enalapril. It thus appears that diminished
vascular responsiveness to NE, especially in the case of captopril, is
probably involved along with converting-enzyme inhibition in the
antihypertensive action of converting enzyme inhibitors (CEI), the
mechanism of the difference between captopril and enalapril remaining still
speculative.
ARTICLES
Effects of captopril and enalapril on regional vascular resistance and reactivity in spontaneously hypertensive rats
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