Captopril attenuates reflex adrenergic response in essential hypertension

An attenuation of adrenergic activity during the inhibition of endogenous angiotensin II formation was evaluated by determining plasma norepinephrine concentration after a single oral administration of captopril compared to that after nifedipine in essential hypertension. Captopril produced a fall in mean arterial pressure (-24 +/- 2 mmHg, p less than 0.01) which magnitude was the same as that gained by nifedipine (-22 +/- 3 mmHg, p less than 0.01). Reflex tachycardia due to hypotension was produced (+13 +/- 1 beats/min, p less than 0.01) after nifedipine but not after captopril (-1 +/- 2 beats/min, p greater than 0.05). Although the enhancement of plasma renin activity induced by captopril (+1.54 +/- 0.56 ng/ml/hr, p less than 0.05) was similar (p greater than 0.05) to that by nifedipine (+1.44 +/- 0.47 ng/ml/hr, p less than 0.05), plasma norepinephrine concentration increased less (p less than 0.01) after captopril (+100 +/- 23 ng/ml, p less than 0.05) than after nifedipine (+283 +/- 51 ng/ml, p less than 0.05). Thus, the diminished adrenergic activity is a likely candidate for the abolished reflex tachycardia after the inhibition of angiotensin I converting enzyme activity by captopril in essential hypertension.