Effects of general and selective beta-adrenergic antagonists on insulin-induced cardiac and selected vascular responses in rats.

Insulin administration results in vasodilation, decreased mean arterial blood pressure (MAP) and increased conductances (flow/MAP) in various vascular beds. beta-adrenergic blockers antagonize this response, but the mechanism of the interplay between insulin-induced vasodilation and beta-adrenergic antagonism is unknown. In this study, we evaluated the effects of beta-blockade using the selective beta(2) antagonist ICI 118551 or the general beta-antagonist propranolol on insulin-induced cardiac and regional flow responses in normal rats. Insulin-induced responses were also examined following adrenalectomy. Rats were anaesthetized and the femoral vein and artery were cannulated for infusions, sampling or monitoring of MAP and heart rate (HR). The iliac, renal, and superior mesentery arteries were equipped with pulsed-Doppler flow probes. Blood samples were collected at selected intervals. Insulin decreased blood glucose, MAP and increased conductances. Pretreatment with propranolol not only antagonized the insulin-induced decrease in MAP and increased conductance but insulin also then increased MAP and decreased conductances. ICI 11851, like propranolol, antagonized the insulin-induced decrease in MAP and increased iliac and renal artery conductances. Adrenalectomy did not alter the maximum insulin-induced effects on MAP and conductances but prevented the rebound recovery phase. beta-blockade following adrenalectomy had the same effects as beta-blockade alone on the insulin-induced responses. We conclude that the insulin-induced decrease in MAP and the increased flow in the selective vascular beds are modulated by a sympathetic beta(2)-receptor-mediated pathway and this response is not due primarily to the release of adrenal catecholamine.