Contribution of cardiac output and peripheral resistance to experimental renal hypertension.

FERRARIO, CARLOS MARIA. Contribution of cardiac output and I periphral resistance to experimental renal hypertension. Am. J. Physiol. 226(3): 71 l-71 7. 1974.-An early increase in cardiac output accompanies development of hypertension due to cellophane perinephritis. The question arose whether a similar hemodynamic response follows rise in blood pressure after constriction of a renal artery. Electromagnetic flowmeters were implanted around the ascending aorta of trained dogs. An externally adjustable clamp was placed around a renal artery 4 wk beforehand. Recordings of aortic blood flow and pressure were obtained in each of 10 dogs for a 20-25 day control period. Cardiac output rose within 48 h after renal artery constriction and remained significantly elevated for up to 28 days in eight dogs developing a benign form of renal hypertension. Rise in peripheral resistance lagged behind the increase in cardiac output, but it then progressively became the predominant cause of elevated blood pressure. These changes were accompanied by an expansion in plasma volume lasting a fortnight. Cardiac output did not increase in the two other dogs, but instead malignant hypertension appeared within 10 days after renal artery constriction; the elevated blood pressure was due to an increased peripheral resistance alone. The experiments indicate that an increase in cardiac output plays an important role in hypertension due to renal artery constriction. The hemodynamic changes are the same as when hypertension is produced by cellophane perinephritis.