We studied the effects of chronic oral inhibition of angiotensin-converting enzyme on the baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate (HR) in 14-wk-old conscious spontaneously hypertensive rats (SHR; n = 12) and age-matched Wistar-Kyoto rats (WKY; n = 11). Rats were treated with lisinopril (10 mg.kg-1.day-1 in tap water) or vehicle for 7 days. We evaluated the baroreflex control of efferent RSNA and HR in awake rats 2 days after implantation of electrodes around the renal sympathetic nerves. The relation between mean arterial pressure (MAP) and either RSNA or HR was analyzed by a logistic function curve during intravenous infusions of phenylephrine and nitroglycerin. The maximum gain of the curve was considered as the sensitivity of the baroreflex. MAP in lisinopril-treated SHR averaged 93 +/- 3 mmHg, a value lower than that obtained in vehicle-treated SHR (147 +/- 5 mmHg) but not in WKY (96 +/- 4 mmHg). In vehicle-treated SHR baroreflex sensitivity (-4.3 +/- 0.5% change nerve activity/mmHg) was significantly (P less than 0.005) smaller than that of WKY (-15.8 +/- 1.5%/mmHg). Seven days of oral treatment of lisinopril caused significant improvement of the baroreflex sensitivity in SHR (-10.5 +/- 0.7%/mmHg, P less than 0.01). The maximum gain of MAP and HR relation of lisinopril-treated SHR was also larger (P less than 0.05) than that of vehicle-treated SHR.(ABSTRACT TRUNCATED AT 250 WORDS)