Whole-Body Circulatory Autoregulation and Hypertension

Abstract

A possible cause of elevated arterial pressure involves the interrelationship between autoregulation of blood flow and control of arterial blood pressure. An autoregulatory response could theoretically result in an elevated arterial pressure and an elevated peripheral resistance with normal or nearly normal cardiac output. Several experimental studies support this theory. Autoregulation of blood flow has been observed in a number of the body's tissues, and the summated effect, whole-body autoregulation, has been demonstrated in areflex dogs. An increase in cardiac output precedes an increase in total peripheral resistance, and a decrease in cardiac output precedes a decrease in total peripheral resistance. The gain of the system was calculated to be slightly greater than three. This same hemodynamic pattern, that is, an increase in cardiac output preceding an increase in resistance, has been observed at the onset of hypertension. We have observed increases in cardiac output at the beginning of salt-induced hypertension in dogs and at the beginning of hypertension secondary to fluid volume expansion in anephric patients, while other investigators have observed this hemodynamic pattern in a number of instances, including labile hypertension, perinephritis hypertension, and Goldblatt hypertension. The increased cardiac output can be caused by several factors, although in many instances the cause appears to be fluid retention. A hemodynamic response suggesting the involvement of whole-body autoregulation, that is, a decrease in cardiac output precedes a decrease in peripheral resistance, has been observed in the reversal of hypertension. Dehydrating overhydrated (and hypertensive) anephric patients and unclipping the renal artery in Goldblatt hypertension elicits this pattern, as well as administration of diuretics or several other antihypertensive drugs to hypertensives. Theoretically, the role of the kidney in hypertension is either to initiate the autoregulatory response by causing fluid retention or to allow the autoregulatory response to occur by preventing the loss of fluid in the face of an elevated arterial pressure.