Responses of the stenosed and contralateral kidneys to [sar¹, thr⁸] all in human reno vascular hypertension

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, [Sar¹, Thr⁸] 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 μEq/min vs 25 ± 9 μEq/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.