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

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Abstract
The role of increased cardiac output in the development of experimental renal hypertension was studied. The studies were made in 5 uninephrectomized, Na-depleted dogs; renal blood flow was reduced by 55-60% 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 l/min to 1.42 and 1.53 l/min (P < 0.05) on days 2 and 4 after RAC. After 4 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 seen. During the control period, PRA was elevated 6- to 8-fold above Na replete values. After RAC, PRA increased transiently on days 2 and 4 and then returned to the high Na-depleted level. Of the 5 dogs 3 were Na repleted 28 days after RAC; arterial pressure was unchanged but CO increased, peripheral resistance fell and PRA returned to the normal level. Apparently Na retention and an increase in cardiac output are unnecessary for the development of 1-kidney experimental renal hypertension and the level of chronic hypertension was unaffected by Na and volume repletion.