Effects of captopril and enalapril on regional vascular resistance and reactivity in spontaneously hypertensive rats.
- 1 May 1983
- journal article
- research article
- Published by Wolters Kluwer Health in Hypertension
- Vol. 5 (3) , 312-320
- https://doi.org/10.1161/01.hyp.5.3.312
Abstract
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.This publication has 37 references indexed in Scilit:
- Attenuation of pressor responses to norepinephrine and pitressin and potentiation of pressor response to angiotensin II by captopril in human subjects.Hypertension, 1982
- Effect of in vitro administration of captopril on vascular reactivity of rat aorta.Hypertension, 1982
- Effects of captopril on vascular reactivity of SHR in vivo and in vitro.Hypertension, 1981
- Preferential noradrenergic innervation of alpha-adrenergic receptors in vascular smooth muscle.Hypertension, 1981
- Effects of long-term blockade of angiotensin converting enzyme with captopril (SQ14,225) on hemodynamics and circulating blood volume in SHR.Hypertension, 1980
- Effect of converting enzyme inhibitor (SQ14,225) on myocardial hypertrophy in spontaneously hypertensive rats.Hypertension, 1980
- Discrepancy between antihypertensive effect and angiotensin converting enzyme inhibition by captopril.Hypertension, 1980
- SQ 14, 225 attenuates the vascular response to norepinephrine in the rat mesenteric arteriesLife Sciences, 1979
- Offset of actions of angiotensin II, angiotensin III, and their analogue antagonists in renal and femoral vascular beds: Further evidence for different vascular angiotensin receptorsLife Sciences, 1979
- Antihypertensive Effect of the Oral Angiotensin Converting-Enzyme Inhibitor SQ 14225 in ManNew England Journal of Medicine, 1978