Cardiovascular reactivity in rats with spontaneous inherited hypertension and constricted renal artery hypertension

Abstract

The cardiovascular responses to pressor drugs and ganglion blockade were examined in rats with spontaneous inherited hypertension and rats with renal hypertension. Similarities and differences in the reactions of the two types of rats were observed. The differences, with other evidence, indicate that the pathogenesis of spontaneous inherited hypertension differs from that of chronic renal hypertension. The blood pressure immediately prior to injection affected the magnitude of the response to vasopressin and angiotensin of rats with inherited hypertension, rats with chronic renal hypertension, and controls at all levels of the blood pressure. Within any one of these groups, higher blood pressures were associated with smaller pressor responses. Therefore, the importance of making allowance for differing levels of blood pressure when one is comparing cardiovascular reactivity is stressed. The responses to vasopressin of rats with inherited hypertension were significantly less than those of renal hypertensive rats with closely comparable blood pressures. The responses of renal hypertensive rats were significantly greater than those of controls. The pressor responses to angiotensin of rats with inherited hypertension, of those with renal hypertension, and of controls did not differ significantly. When the initial blood pressures were less than 170 mm. Hg (the upper level of blood pressures commonly encountered in rats with inherited hypertension), the responses to norepinephrine of rats with inherited hypertension, of those with renal hypertension, and of controls showed no correlation with the blood pressure and did not differ significantly. In renal hypertensive rats with blood pressures greater than 170 mm. Hg the pressor responses to norepinephrine decreased with increasing blood pressure. After ganglion blockade with hexamethonium the blood pressure fell to a significantly lower level in rats with inherited hypertension than in rats with renal hypertension, and in both cases the blood pressure after hexamethonium was higher than that of control rats. The extent of the fall was dependent on the initial level of the blood pressure. The neurogenically maintained component of the blood pressure which was removed by ganglion blockade was mainly responsible for the elevation of the blood pressure to hypertensive levels in rats with inherited hypertension. At closely similar levels of the blood pressure the neurogenically maintained fraction of the blood pressure accounted for approximately 60 per cent of the elevation of the blood pressure above control levels in rats with inherited hypertension, and for only 30 per cent of the excess in renal hypertensive rats.