Responses of the stenosed and contralateral kidneys to [Sar1, Thr8] AII in human renovascular hypertension.

Abstract

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...

Effects of converting enzyme inhibition on split renal function in renovascular hypertension.

“…The hemodynamic changes in the nonstenotic kidneys were similar to those seen in patients with EH. Textor et al, 9 using the angiotensin II analogue [Sar'.Thr 8 ] angiotensin II, have reported a striking heterogeneity in the renal hemodynamic responses of patients with RVH depending on baseline PRA. The variability in the response was partly attributable to the agonistic action of the analogue.…”

“…18 In the patients with EH, captopril did not affect GFR but slightly increased ERPF in both kidneys. Previous evidence indicated that the renal vasculature is sensitive to angiotensin II' 9 and that the arterial resistance is increased in patients with EH. 20 Hence, it is conceivable that captopril decreases vascular resistance in patients with EH by inhibiting angiotensin II formation.…”

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“…GFR and RPF were determined by simultaneous clearance measurements of '251-iothalamate and l3lIiodohippurate, respectively, according to the method described by Textor and co-workers (25 where UNa+ and SNa+ are the concentrations of sodium ion in mEq/L in the urine and plasma, respectively, and Ucr and Scr are concentrations of creatinine in mg/dl in the urine and plasma, respectively. Free water clearance (CHz0) was defined and calculated as V X (1 -Uosm/Posm) where V is urine output rate in ml/min/kg.…”

An Update on Renovascular Hypertension

“…The contralateral (nonstenotic) kidney exhibits suppressed production of renin [9]. In the initial phase of this setting, the direct pressor effect of angiotensin II seems to be a dominant mechanism of RVH [10].…”