Abstract
Reflex activation of the sympathetic nervous system may conceal direct vasodilatory actions of atrial natriuretic factor and mediate atrial natriuretic factor-induced increases in total peripheral resistance. We determined whether peripheral sympathectomy would enhance the hypotensive actions of atrial natriuretic factor and convert the increase in total peripheral resistance to peripheral vasodilation. Sympathectomized rats studied included 1) conscious rats treated with 6-hydroxydopamine alone (partially sympathectomized) and 2) conscious anephric rats sympathectomized with adrenal demedullation and 6-hydroxydopamine (totally sympathectomized), with vascular tone returned to levels of sham-operated (control) rats with norepinephrine infusion. Sympathectomized rats and appropriate control rats received rat atrial natriuretic factor infusion (0.5 microgram/kg/min) or vehicle for 1 hour. Atrial natriuretic factor infusion lowered mean arterial pressure and increased hematocrit in control rats but not in partially sympathectomized rats. Changes in cardiac output and total peripheral resistance were not significantly different between control and partially sympathectomized rats. In totally sympathectomized rats, atrial natriuretic factor lowered mean arterial pressure more than in control rats; changes in cardiac output were nearly identical in both groups, but there were no changes in total peripheral resistance from control levels in the totally sympathectomized group. Changes in plasma volume and central venous pressure were similar in totally sympathectomized rats and control rats. These findings suggest that reflex sympathetic activity largely mediated atrial natriuretic factor-induced increases in total peripheral resistance but failed to reveal an atrial natriuretic factor-mediated sustained vasodilation in the absence of sympathetic reflexes. Furthermore, atrial natriuretic factor decreased cardiac output, central venous pressure, and plasma volume independent of the sympathetic nervous system.
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