SUMMARY To better define the intrarenal hemodynamic effects of anglotensin in human renovascular hypertension, 10 patients underwent renal hemodynamic and functional measurements before and during infusion of a competitive angiotensin analog, [Sar 1 , Thr 8 ] AIL Eight had technically satisfactory split function studies. Despite a fall in mean arterial pressure (132 ± 6 to 121 ± 6 mm Hg, p < 0.05) and humoral changes consistent with angiotensin-mediated hypertension, the intrarenal effects of this analog were commonly those of an angiotensin agonist, producing vasoconstriction and sodium retention. This was quantitatively greatest in the contralateral kidney, whose preinfusion sodium excretion (86 ± 30 /xEq/min vs 25 ± 9 /xEq/min, p < 0.02) and glomerular filtration rate (76 ± 7 ml/min vs 41 ± 7 ml/min, p < 0.01) were higher than the stenotic kidney. In some cases, an increase in renal blood flow and rise in sodium excretion were evident during angiotensin blockade, suggesting a tonic intrarenal action of angiotensin. Although renin vein renin values differed markedly between the stenotic and contralateral kidney (ratio = 2.05 ± 0.30), relative changes in effective renal plasma flow were correlated (r = 0.84; p < 0.01) during infusion of this analog. These results underscore the differences in sensitivities between vascular beds to the effects of angiotensin II and the major role of the contralateral kidney in renal function and sodium homeostasis in human renovascular hypertension. (Hypertension 5: 796-804, 1983) KEY WORDS * [Sar 1 , Thr 8 ] AH • renovascular hypertension • angiotensin antagonists • renal hemodynamics A LTHOUGH unilateral renal artery stenosis regularly produces hypertension in both animals and humans, the relative roles of the stenotic and contralateral kidney in this process remain incompletely defined. It has been suggested that the unaffected kidney may play a contributory role by failing to excrete salt and water despite rising arterial pressure.1 " 4 Several lines of evidence do suggest, in fact, that sodium retention participates in human renovascular hypertension. Intravascular volume measurements are no different from those observed in essential hypertension.5 Second, "angiotensin-dependence" of blood pressure as defined by changes induced by interruption of the renin-angiotensin system by competitive antagonists may not be evident without prior administration of diuretics.6 " 8 Third, demonstration of lateralization of renal vein renin production to the stenotic side often requires prior sodium depletion.
9From the Research Division and Department of Urology, Cleveland Clinic Foundation, Cleveland. Ohio.Presented at the 14th Annual Session of the American Society of Nephrology, Washington, D.C., November 22-24, 1981. Received December 15, 1982 revision accepted April 15, 1982. Experimental studies in renovascular (two-kidney, one clip) hypertension have demonstrated functional changes in the contralateral kidney (CLK), which is often hypertrophied due to the reduction of nephro...