LONG-TERM CAPTOPRIL TREATMENT RESTORES NATRIURESIS AFTER CAROTID BARORECEPTOR ACTIVATION IN THE SHR

In anesthetized Sprague-Dawley rats, intermittent bilateral carotid ar tery traction (BilCAT) caused a transient decrease in mean arterial pr essure (MAP) of 28 +/- 3 mmHg and led to a progressive increase in sod ium excretion (UNaV) that nearly doubled 45-90 min after initiation of the repetitive application of BilCAT (P < 0.001). This natrinresis wa s accompanied by an increase in glomerular filtration rate (GFR) from 2.70 +/- 0.3 to 3.2 +/- 0.3 ml/min (P < 0.001), no change in renal pla sma flow [clearance of p-aminohippurate (PAH)], and an increase in the fractional excretion of lithium. Rats with bilateral renal denervatio n exhibited neither natriuresis nor an increase in GFR in response to BilCAT despite similar vasodepression caused by the maneuver. Normoten sive Wistar-Kyoto (WKY) rats responded to BilCAT like Sprague-Dawley r ats, whereas spontaneously hypertensive rats (SHR) exhibited an exagge rated vasodepressor response to BilCAT (-51 +/- 3 mmHg) without increa sing either UN,V or GFR. Separate groups of WKY and SHR were treated f rom 4 wk of age with captopril added to the drinking water at a concen tration of 1 g/l. At 12-14 wk, both groups had lower MAP compared with untreated animals. Captopril treatment did not alter either the natri uretic response or the increase in GFR seen in untreated WIN after Bil CAT, and the maneuver produced equivalent degrees of vasodepression as in controls. However, treated SHR now responded to BilCAT with. incre ases in both UNaV and GFR that closely resembled the responses seen in Sprague-Dawley and WKY rats. These results suggest that BilCAT produc es natriuresis through a pathway dependent on the renal nerves. This p athway does not function in untreated SHR despite similar vasodepressi on. Long-term treatment with captopril restores this reflex pathway in SHR, lending support to the concept that angiotensin II is critically Linked to heightened sympathetic nerve activity and abnormal sodium m etabolism in this strain.