ENDOGENOUS ANGIOTENSIN-II FACILITATES SYMPATHETICALLY MEDIATED HEMODYNAMIC-RESPONSES IN PITHED RATS

  • 1 January 1985
    • journal article
    • research article
    • Vol. 235  (1) , 128-134
Abstract
The influence of endogenous angiotensin III on the hemodynamic responses to electrical stimulation of the sympathetic outflow was assessed in pithed male normotensive Wistar rats fitted with aortic flow probes for continuous measurement of cardiac output (CO). The frequency-related increments (0.25-4.0 Hz) in blood pressure (BP) and total peripheral resistance (TPR) were significantly attenuated by treating animals with the angiotensin converting enzyme inhibitor captopril (5 mg/kg i.v.) or the angiotensin II receptor antagonist saralasin (10 .mu.g/kg/min i.v.). However, the increments in CO and heart rate during neural stimulation were unaffected by blockade of the renin-angiotensin system. After captopril treatment, infusion of angiotensin II (40 ng/kg/min i.v.) to replace the loss of endogenous angiotensin II restored stimulation-induced TRP and BP responses toward precaptopril levels; CO and heart rate responses to stimulation were not altered. The hemodynamic responses to exogenous norepinephrine were affected by inhibition of the renin-angiotensin system with captopril and saralasin in a manner analogous to the neurally mediated responses. The results obtained with nerve stimulation and norepinephrine indicate that endogenos angiotensin II selectively interacted with sympathetic neural control of vascular resistance, whereas cardiac responsiveness to noradrenergic neurons was not altered. Moreover, in the absence of nerve stimulation, the antagonism of the renin-angiotensin system lowered base-line BP by reducing CO without measurably affecting TPR. Infusion of angiotensin II reversed these effects and restored BP toward precaptopril levels by increasing CO without measurably affecting TPR. Thus, endogenous angiotensin II appears to contribute to the maintenance of BP in the pithed animal by decreasing venous capacitance, thereby maintaining CO. Only when sympathetic discharge was superimposed was the contribution of angiotensin II to TPR readily apparent. Thus the hemodynamic effects of the sympathetic nervous system are markedly dependent on circulating levels of angiotensin II.

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