The role of β2-adrenergic vascular receptors in the peripheral vasodilation caused by 17β-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 coronary circulations, while higher doses of the hormone were required to cause vasodilation also in the mesenteric vascular bed. In the same experimental model, a tonic beta(2)-adrenoceptor mediated vasodilation, which could be argued to attenuate the vasodilator effect of 17 beta-estradiol, has been described. The present study was planned to investigate the role of beta(2)-adrenergic receptors in the hemodynamic responses of renal and mesenteric vascular beds to 17 beta-estradiol. Changes in flow caused by intravenous infusion of 2 mu g/h of the hormone at constant heart rate and aortic, blood pressure in the left renal and superior mesenteric arteries were assessed using electromagnetic flowmeters. In six pigs, infusion of 17 beta-estradiol caused an increase in renal blood flow, which averaged 12.1% of the control values, without affecting mesenteric blood flow. In the same pigs, after hemodynamic variables had returned to the baseline values, blockade of beta(2)-adrenergic receptors with butoxamine caused gn increase in aortic blood pressure and an increase in renal and mesenteric resistance. The subsequent infusion of 17 beta-estradiol elicited increases in renal and mesenteric blood flow which respectively averaged 19.6% and 12.8%. Therefore, the present study in anesthetized pigs have shown that the vasodilator responses of the renal and mesenteric circulations to 17 beta-estradiol were attenuated and even masked by a tonic beta(2)-adrenoceptor mediated vasodilation. This indicates that some vasodilator effects elicited by normally used replacement doses of the hormone may not be apparent.