Autonomic and baroreflex function after captopril in hypertension

Absent reflex tachycardia with captopril therapy suggests blunting of circulatory reflexes, perhaps contributing to antihypertensive efficacy, and angiotensin converting enzyme inhibition may alter sympathetic function. Captopril effects on autonomic function were investigated in five severe hypertensive patients. Mean blood pressure fell in all patients (from 141 ± 6 to 119 ± 7 mm Hg, p < 0.02) without orthostatic blood pressure fall or increase in heart rate (both p > 0.1) on captopril. Captopril did not alter baroreflex sensitivity as tested by amyl nitrite hypotension or phenylephrine hypertension (both p > 0.1). Comparison of these severely hypertensive patients to age matched normotensive control subjects did reveal markedly blunted baroreflex sensitivity in both the amyl nitrite test (by 89%, p < 0.01) and the phenylephrine test (by 83%, p < 0.01), suggesting that baseline blunting of baroreflex function may in part account for absence of reflex tachycardia. Captopril diminished the cardioacceleration after cold stress (from 61 ± 38 to 23 ± 43 msec, p < 0.05) as well as the blood pressure fall after alpha-adrenergic blockade (from 46 ± 13 to 24 ± 9 mm Hg, p < 0.05), suggesting diminished sympathetic stimulation of resistance vessels and decreased sympathetic participation in blood pressure maintenance, possibly at the prejunctional synpatic level. Four biochemical indices of sympathetic activity did not change. Thus captopril-treated patients had blunted reflex tachycardia, commensurate with blunted baroreflex function at baseline, and physiologic and pharmacologic evidence of diminished sympathetic activity was obtained with captopril therapy. Whether diminished sympathetic activity is involved in captopril's antihypertensive effect has not been determined.