The antihypertensive effect of captopril on L-NAME-induced acute hypertension in rats is partly dependent on the potentiation of bradykinin's vasodilator actions.
Supports bradykinin-dependent captopril action in L-NAME rat models; leaves open translation to human hypertension therapy.
The aim of the present study was to investigate the role of bradykinin in the inhibitory action of captopril in hypertension induced by L-NAME in anesthetized rats. Male Wistar rats (260-320 g) were anesthetized with chloralose and arterial blood pressure was recorded with a polygraph pressure transducer. The hypertensive effect of L-NAME was studied in rats pretreated with saline, captopril or HOE 140 plus captopril. The effect of captopril was also studied during the sustained pressor effect of L-NAME. The acute pressor effect of L-NAME (10 mg/kg, i.v.) was significantly reduced by i.v. pretreatment with 2 mg/kg captopril (delta increase of 49 +/- 4.9 mmHg reduced to 20 +/- 5.4 mmHg, P = 0.01). The pressor effect of L-NAME (delta increase of 38 +/- 4.8 mmHg) observed in rats pretreated with captopril and HOE 140 (0.1 mg/kg, i.v.) was not significantly different from that induced by L-NAME in rats pretreated with saline (P = 0.09). During the sustained pressor effect induced by L-NAME (delta increase of 49 +/- 4.9 mmHg) captopril induced a significant (P < 0.05) reduction in arterial blood pressure (delta decrease of 22 +/- 3.0 mmHg). The present results demonstrate that the acute pressor effect of L-NAME is reduced by captopril and this inhibitory effect may be partly dependent on the potentiation of the vasodilator actions of bradykinin.
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Moura et al. (1997) studied this question.
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