TRACHEAL MICROVASCULAR RESPONSES TO BETA-ADRENERGIC STIMULATION IN ANESTHETIZED RATS

Previous study of adrenergic control of the tracheal vasculature in ra ts (1) demonstrated that beta-adrenergic blockade heightened arteriola r and large venular contractile responses to norepinephrine, a nonsele ctive alpha-adrenergic agonist. The present study was undertaken to co nfirm the presence of functional beta-adrenergic receptors and to dete rmine which beta-adrenergic receptor subtypes mediate vasodilation in this tissue. Tracheal adventitial arterioles (12.0 to 47.0 mu m initia l diameter, n = 39) and venules (48.0 to 98.5 mu m initial diameter, n = 44) were observed through a video microscope, and vessel diameters were measured. Vessels were preconstricted with 10(-4) M phenylephrine (PHE), a selective alpha(1)-adrenergic agonist, to achieve sufficient tone for measurement of dilation responses. When vessels were treated only with PHE, arterioles and venules constricted to 55.9% and 67.6% of their initial diameter, respectively, after 15 min of suffusion. Wh en preconstricted vessels were treated with the nonselective beta-adre nergic agonist isoproterenol (10(-5) M), both arterioles and venules s ignificantly dilated from 63.4% to 82.9% and from 71.5% to 81.3% of th eir initial diameters. At high concentration (10(-5) M), the putative beta(2)-adrenergic agonist terbutaline also caused preconstricted arte rioles and venules to significantly dilate from 70.8% to 79.8% and fro m 71.5% to 83.4% of their initial diameters. The selective beta(1)-adr energic antagonist atenolol (10(-6) M) did not affect terbutaline-indu ced dilation in preconstricted arterioles, but greatly attenuated dila tion in preconstricted venules. From these data, we conclude that beta (2)-adrenergic receptors are present in and mediate dilation of trache al arterioles, and also, that the dilation in large tracheal venules i s mediated in large part through beta(1)-adrenergic receptors.