PubMed1982
Captopril (SQ 14225) is an orally active agent that inhibits the conversion of ang. I to ang. II and also potentiates the biological actions of kinins. This substance has been used to study the role of ang. II/kinins on the norepinephrine-induced vasoconstriction in the isolated perfused mesentery and hindquarters of the rat. The vasoconstrictor responses were measured as an increase in the perfusion pressure (mm Hg), induced by sequential injections of norepinephrine. Captopril/placebo (physiological saline solution) was administered in a dose of 1 mg/kg by oral route, 15-20 min before isolating the vascular beds from these rats. Oral administration of captopril, decreased the vascular reactivity to norepinephrine in both the vascular beds, when compared to the responses obtained in the placebo treated rats. In another series of experiments (normal rats) bradykinin (BK), at concentrations of 0.4 and 0.8 micrograms/ml in the perfusate, attenuated the norepinephrine-induced vasoconstriction dose dependently, only in the mesenteric bed. It may be concluded that captopril attenuated the vascular reactivity to norepinephrine either by decreasing ang. II formation and/or increasing the action of kinins in the vicinity of these two beds. The latter mechanisms, however, appears not to play any direct role in the hindquarter bed. The direct effects of captopril on the decreased vascular reactivity of these beds cannot, however, be ruled out.