Diminished sympathetic responsiveness in nephrectomized rats-role of the renin angiotensin system.

Experiments were conducted in pithed Wistar rats to assess the effects of nephrectomy on the responsiveness of the cardiovascular system to sympathetic neurohumoral stimuli. Blood pressure and heart rate increases produced in response to stimulation of the spinal sympathetic outflow and to norepinephrine were compared in nephrectomized (NXR) and sham operated animals (SOR). Both the blood pressure (BP) and heart rate (HR) increases to nerve stimulation were markedly attenuated in the NXR, however, only the reduction in BP responses could be attributed to the absence of a functional renin angiotensin system. Infusion of angiotensin II (10 ng/kg/min) in NXR enhanced the neurally mediated increments in BP to the extent that the responses were not different from SOR. Angiotensin II administration also enhanced BP responses in SOR but to a lesser extent than in NXR. HR responses were not altered by angiotensin in NXR or SOR. Blockade of the renin angiotensin system in SOR with the converting enzyme inhibitor, captopril, reduced BP responses to the same level as NXR. In contrast, HR increments were not altered by captopril. BP but not HR increments to norepinephrine were significantly reduced in NXR. Infusion of angiotensin II restored the BP responses to a level equal to SOR; HR responses were not affected. In addition, captopril reduced the norepinephrine responses of SOR but not NXR. Thus the results of the present study indicate that endogenously formed angiotensin facilitates sympathetically mediated vasoconstrictor activity but does not influence heart rate responses. Therefore, the attenuation of neurally elicited increases in HR observed in NXR does not appear to be acutely related to reduced levels of angiotensin II.