Baroreflex Modifies the Effect of Vasodilators on Systemic Capacitance Vessel in Dogs

Abstract

We examined whether the vasodilating effect of vasodilators on systemic capacitance vessels is modified by the baroreflex when a fall in arterial blood pressure was induced by the vasodilators in dogs. We estimated the dilation of the systemic capacitance vessels from the fall in mean circulatory pressure (MCP), proposed by Guyton et al. and the dilation of the systemic capacitance vessels from the fall in the total peripheral resistance (TPR). The dose-response curve for percent change in TPR to graded doses of nitroglycerin (NG, 0.8–200 µg/kg) in the untreated group was not different from that in the total spinal anesthesia (TSA) group in which the baroreflex was eliminated. The TSA group gave a dose-response curve for percent change in MCP to NG on the low dose side of NG as compared with the untreated group. NG increased both plasma levels of nor-epinephrine (NA) and epinephrine (A) in the untreated group. However, NG hardly affected plasma levels of NA or A in the TSA group. Milrinone significantly decreased the TPR and there was no significant difference in the percent change in TPR between the untreated and TSA groups. Milrinone did not change the MCP in the untreated group, but decreased it in both TSA group and the group pretreated with α-blocker, suggesting that baroreflex-mediated vasoconstriction is mediated through α-adrenoceptors in the capacitance vessels. Milrinone also increased plasma levels of NA and A in the untreated group but not in the TSA group.

These results suggest that the administration of vasodilators, which induces strong and rapid dilation of systemic resistance vessels, causes the baroreflex, and that the vasodilating effect of vasodilators on the systemic capacitance vessels is strongly modified by this baroreflex-mediated venoconstriction.