Short- and long-term enalapril affect renal medullary hemodynamics in the spontaneously hypertensive rat

Long-term angiotensin-converting enzyme (ACE) inhibition in the spontaneous ly hypertensive rat (SHR) resets pressure natriuresis and shins the relatio nship between renal arterial pressure (RAP) and renal interstitial hydrosta tic pressure (RIHP) to lower levels of arterial pressure. These effects per sist after withdrawal of treatment. The purpose of this study was to determ ine the effect of short- and long-term ACE inhibition on medullary blood fl ow (MBF). Enalapril (25 mg.kg(-1).day(-1) in drinking water) was given to m ale SHR from 4 to 14 wk of age. Four weeks after stopping treatment, we mea sured MBF over a wide range of RAP using laser-Doppler flowmetry in anesthe tized rats, additional rats, either untreated or previously treated for 10 wk, received a-day enalapril treatment just before the experiment. MAP (mmH g +/- SE) was 178 +/- 6 (n = 8), 134 +/- 6 (n = 8), 138 +/- 5 (n = 9), and 111 +/- 6 mmHg (n = 9) for the untreated, 3 day, 10 wk, and 10 wk + 3 day g roups, respectively. Total renal blood flow for the groups receiving S-day treatment was significantly higher when compared with that in rats with an intact renin-angiotensin system. Three-day treatment had no effect on the r elationship between RAP and RIHP, whereas that in rats receiving 10-wk trea tment was shifted to lower levels of RAP by similar to 30 mmHg. Both 10-wk and S-day treatment independently increased the slope of the RAP versus MBF relationship at values of RAP > 100 mmHg. The slopes in perfusion units/mm Hg were 0.12 +/- 0.01 (n = 8), 0126 +/- 0.01 (n = 8), 0.27 +/- 0.01(n = 9), and 0.30 +/- 0.02 (n = 9) for the untreated, 3 day, 10 wk, and 10 wk + 3 d ay groups, respectively. These results indicate that the effect of short-te rm and the persistent effect of long-term enalapril alter renal medullary h emodynamics in a way that may contribute to the resetting of the pressure-n atriuresis relationship in treated rats.