Increased Cardiac Output as a Contributory Factor in Experimental Renal Hypertension in Dogs

Abstract

It has been suggested, but not established, that renal hypertension is initiated by increase incardiac output. Recent refinements in electromagnetic flowmeter technology allowed a critical reevaluation of this possibility. Flowmeters were implanted around dogs' ascending aortas and arterial catheters inserted; measurements were made daily before and after production of hypertension by the cellophane perinephritis method. Eight to 15 days after wrapping one kidney in cellophane, with the opposite kidney untouched, group averages for both stroke volume and cardiac output rose significantly (P < 0.005) though there was no change in arterial pressure. Both heart rate and peripheral resistance decreased slightly. Following these measurements, the contralateral normal kidney was removed and measurements were recommenced 24 hours later. After 4 to 7 days, mean arterial pressure rose progressively in all dogs, reaching a plateau 77 ± 8 (SE) mm Hg above control after 14 to 25 days. Hypertension was associated initially with further rise in both stroke volume and cardiac output, and peripheral resistance now became elevated. Four weeks after nephrectomy, peripheral resistance progressively became the predominant cause of elevated pressure while cardiac output returned toward control values. Absence of change in plasma volume and increase in mean circulatory pressure measured in a separate series of 7 dogs suggest that the initial increase in cardiac output preceding rise in pressure was due to enhanced venous return consequent to constriction of capacitance vessels. We conclude that increased cardiac output probably has a contributory role in the development of renal hypertension.