The role of beta(2)-adrenergic vascular receptors in the peripheral vasodilation caused by 17 beta-estradiol in anesthetized pigs

It has been previously shown in anesthetized pigs that intravenous infusion of 2 mu g/h of 17 beta-estradiol primarily dilated renal, iliac and corona ry circulations, while higher doses of the hormone were required to cause v asodilation also in the mesenteric vascular bed. In the same experimental m odel, a tonic beta(2)-adrenoceptor mediated vasodilation, which could be ar gued to attenuate the vasodilator effect of 17 beta-estradiol, has been des cribed. The present study was planned to investigate the role of beta(2)-ad renergic receptors in the hemodynamic responses of renal and mesenteric vas cular beds to 17 beta-estradiol. Changes in flow caused by intravenous infu sion of 2 mu g/h of the hormone at constant heart rate and aortic, blood pr essure in the left renal and superior mesenteric arteries were assessed usi ng electromagnetic flowmeters. In six pigs, infusion of 17 beta-estradiol c aused an increase in renal blood flow, which averaged 12.1% of the control values, without affecting mesenteric blood flow. In the same pigs, after he modynamic variables had returned to the baseline values, blockade of beta(2 )-adrenergic receptors with butoxamine caused gn increase in aortic blood p ressure and an increase in renal and mesenteric resistance. The subsequent infusion of 17 beta-estradiol elicited increases in renal and mesenteric bl ood flow which respectively averaged 19.6% and 12.8%. Therefore, the presen t study in anesthetized pigs have shown that the vasodilator responses of t he renal and mesenteric circulations to 17 beta-estradiol were attenuated a nd even masked by a tonic beta(2)-adrenoceptor mediated vasodilation. This indicates that some vasodilator effects elicited by normally used replaceme nt doses of the hormone may not be apparent.