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We evaluated the role of increased cardiac output in the development of experimental renal hypertension. The studies were made in five uninephrectomized, sodium-depleted dogs; renal blood flow was reduced by 55-00% by renal artery constriction (RAC). Blood pressure (BP), plasma renin activity (PRA), heart rate (HR), cardiac output (CO), stroke volume (SV), and plasma volume (PV) were determined in conscious dogs before and on days 2, 4, 6, 10, 14, 21, and 28 after RAC. After RAC, BP increased from a control mean value of 96 mm Hg to 118-147 mm Hg. CO fell from a control mean value of 1.92 liters/min to 1.42 and 1.63 liters/min (P < 0.05) on days 2 and 4 after RAC. After four days of RAC, CO was not significantly different from the control mean value. During hypertension, HR was consistently lower than the control mean value of 94 beats/min. Water balance was positive on days 1 and 4, but no change in PV was detected. During the control period, PRA was elevated ft- to 8-fold above sodium replete values. After RAC, PRA increased transiently on days 2 and 4 and then returned to the high sodium-depleted level. Three of the five dogs were sodium repleted 28 days after RAC; arterial pressure was unchanged but CO increased, peripheral resistance fell, and PRA returned to the normal level. The results demonstrate that sodium retention and a consequent increase in cardiac output were unnecessary for the development of one-kidney experimental renal hypertension. Also, the level of chronic hypertension was unaffected by sodium and volume repletion. cire Res 44: 316-321, 1979

Hemodynamic, fluid, and electrolyte changes in sodium-depleted, one-kidney, renal hypertensive dogs.