The renal artery to a sole remaining kidney was constricted in unanesthetized dogs while renal arterial pressure was recorded distal to the occluder. Following the constriction, mean arterial blood pressure, which was continuously monitored 24 hours a day for 1 week, exhibited a biphasic increase. The first peak in pressure correlated with a large increase in plasma renin activity; the second peak correlated with an increase in plasma volume brought about by positive sodium and water balances. Renin activity was returning to normal when the second peak occurred. Increased drinking played a major role in the positive water balance. Plasma aldosterone concentration was moderately and transiently increased for only a few hours following the constriction. The experiment was repeated in sinoaortic baroreceptor-denervated dogs; apparently, the baroreceptor reflex significantly slows the time course of the arterial blood pressure increase during the first few days of constriction but does not alter the magnitude of the pressure increase after 1 week. After release of renal artery constriction, mean arterial blood pressure decreased progressively over a 3-day period, during which time significant negative sodium and fluid balance occurred. The slow return of the pressure back to normal correlated highly with a decrease in plasma volume. In the baroreceptor-denervated dogs, the initial fall in arterial blood pressure apparently also resulted at least partly from a decrease in plasma renin activity, but this effect was not observed in the intact dogs because the renin activities in these dogs had already decreased to normal prior to constrictor release. The effects of the baroreceptor reflex on the time course of the pressure decrease did not seem to be as significant as those on the time course of the pressure increase. KEY WORDSarterial blood pressure heart rate sodium space sodium potassium continuous data collection fluid balance studies plasma volume• The magnitude and the time course of the increase in mean arterial blood pressure following constriction of the renal artery to a sole remaining kidney (Goldblatt hypertension) depend on the interaction of a number of mechanisms: the release of renin by the kidney (1, 2), the retention of sodium and water, the expansion of fluid volumes (1, 3-6), the buffering action of the baroreceptor reflexes, and still other arterial blood pressure control systems are all involved. However, few studies

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The nephrectomized patient maintained on intermittent hemodialysis while awaiting renal transplantation provides an excellent model for studying the influence of factors other than the renal renin-angiotensin system that play a role in the regulation of plasma aldosterone concentration. Peripheral plasma aldosterone concentrations were determined using a sensitive radioimmunoassay method in nine anephric patients in the recumbent position immediately before and after hemodialysis. Average patient weight fell 1.5 kg following 12 hours of dialysis on the Kiil dialyzer. Plasma sodium concentration decreased from 137 ± 1 (SE) to 132 ± 1 mEq/ liter, plasma potassium concentration decreased from 4.8 ± 0.3 to 3.2 ± 0 . 1 mEq/liter, and the ratio of sodium to potassium increased from 31.3 ±1.9 to 41.7 ± 0.9. Plasma aldosterone concentration increased from 9.7 ± 1.6 ng/100 ml plasma before dialysis to 17.9 ± 2 . 1 ng/100 ml plasma after dialysis despite the lack of kidneys to produce renin. Plasma cortisol concentration did not change significantly (17.5 ± 2 . 0 /ig/100 ml plasma to 14.8 ± 1.9 yug/100 ml plasma). These results show that plasma aldosterone concentration increased in anephric patients in response to hemodialysis. This increase occurred without a concomitant increase in plasma cortisol levels, suggesting absence of an adrenocorticotropic hormone response, and was independent of the renal reninangiotensin system.

The aldosterone response to long-term infusion of angiotensin II and potassium was studied in intact conscious dogs. Plasma aldosterone concentration (PAC), plasma renin activity (PRA), and plasma cortisol concentration (PCC) were determined by radioimmunoassay. In ten dogs maintained on angiotension II infusion (5 ng/kg min-1) for 14 days, PAC increased from 6.9 plus or minus 2.9 to 18.6 plus or minus 4.7 ng/100 ml plasma (mean plus or minus SE) within ten minutes after beginning the infusion, reached a maximum level of 28.3 plus or minus 6.8 ng/100 ml plasma by one hour, and returned to control levels by six hours. PCC increased from 0.6 plus or minus 0.2 to 3.9 plus or minus 1.0 mu-g/ 100 ml plasma within one hour after angiotensin II infusion and returned to control levels by six hours. During the next 14 days of angiotensin infusion, PAC remained at control levels, PRA was undetectable by radioimmunoassay, and mean arterial blood pressure was elevated 29 plus or minus 4 mm Hg above control levels. In ten dogs maintained on KCL infusion (250 mEg/day) for 15 days, PAC increased from 6.8 plus or minus 2.4 to 13.6 plus or minus 3.4 ng/100 ml plasma within 24 hours, averaged 22.4 plus or minus 4.3 ng/100 ml plasma by 48 hours, and remained elevated for the next 12 days, averaging 21.8 plus or minus 5.6 ng/100 ml plasma. During the next 14 days of KCL infusion, serum Kn increased from 4.1 plus or minus 0.3 to 4.9 plus or minus 0.5 ME1/L, and PRA decreased from 1.25 plus or minus 0.3 to 0.65 plus or minus 0.2 ng/ml/hr. PCC averaged 0.73 plus or minus 0.4 mu-g/100 ml plasma in the control samples and failed to change significantly during KCL infusion. These data indicate that chronic angiotensin II infusion into intact conscious dogs at rates capable of maintaining elevated arterial blood pressure results in a transient increase in aldosterone secretion that lasts only a few hours, while chronic infusion of potassium ions at rates that produce a minor increase in serum Kn results in a sustained increase in aldosterone secretion.