RENAL EFFECTS OF ANGIOTENSIN-II INHIBITION DURING INCREASES IN RENAL VENOUS-PRESSURE

Increases in renal venous pressure have been shown to consistently increase renal interstitial pressure; however, not until renal interstitial pressure is increased threefold is a natriuresis noted in normal animals. Since the intrarenal angiotensin II (Ang II) concentration has been postulated to increase with increasing renal venous pressure, the antinatriuretic action of Ang II could override the natriuretic effect of increased renal interstitial pressure. Therefore, the role of Ang II in the natriuretic response to increased renal venous pressure was examined in 10 pentobarbital-anesthetized dogs. Mean arterial pressure, renal blood flow, renal interstitial pressure, glomerular filtration rate, urinary sodium excretion, plasma renin activity, and prostaglandin E2 excretion were measured at renal venous pressures of 3, 15, and 30 mm Hg. The measurements were repeated after the administration of captopril (1 mg/kg i.v. bolus, n = 5) or [Sar1,IIe8]Ang II (50-mu-g/kg i.v. bolus + 50-mu-g/kg/hr infusion, n = 5). Under control conditions, mean arterial pressure, renal blood flow, plasma renin activity, and prostaglandin E2 excretion remained unchanged when renal venous pressure was increased. The elevations in renal venous pressure increased renal interstitial pressure from 7 +/- 2 to 12 +/- 2 and 22 +/- 4 mm Hg, while sodium excretion remained unchanged until renal venous pressure was 30 mm Hg. In the captopril-treated group, increasing renal venous pressure increased renal interstitial pressure as under control conditions; however, sodium excretion (23 +/- 4, 19 +/- 4, and 27 +/- 6-mu-eq/min) was not significantly increased even at the highest renal venous pressure. In the presence of [Sar1,IIe8]Ang II, increasing renal venous pressure increased renal interstitial pressure as before administration of the antagonist while sodium excretion did not change significantly (7 +/- 3, 7 +/- 2, and 16 +/- 4-mu-eq/min), even at the highest renal venous pressure. The withdrawal or inhibition of Ang II failed to potentiate the natriuretic effect of increased renal interstitial pressure at renal venous pressures of 15 and 30 mm Hg. The inability of the kidney to maintain the glomerular filtration rate at high venous pressures may have contributed to the lack of natriuresis.