Tracheal microvascular responses to beta-adrenergic stimulation in anesthetized rats.
Previous study of adrenergic control of the tracheal vasculature in rats (1) demonstrated that beta-adrenergic blockade heightened arteriolar and large venular contractile responses to norepinephrine, a nonselective alpha-adrenergic agonist. The present study was undertaken to confirm the presence of functional beta-adrenergic receptors and to determine which beta-adrenergic receptor subtypes mediate vasodilation in this tissue. Tracheal adventitial arterioles (12.0 to 47.0 micro m initial diameter, n=39) and venules (48.0 to 98.5 micrometers 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. When preconstricted vessels were treated with the nonselective beta-adrenergic agonist isoproterenol (10(-5) M), both arterioles and venules significantly dilated from 63.4% to 82.9% and from 71.5% to 81.3% of their initial diameters. At high concentration (10(-5) M), the putative beta 2-adrenergic agonist terbutaline also caused preconstricted arterioles and venules to significantly dilate from 70.8% to 79.8% and from 71.5% to 83.4% of their initial diameters. The selective beta 1-adrenergic antagonist atenolol (10(-6) M) did not affect terbutaline-induced dilation in preconstricted arterioles, but greatly attenuated dilation in preconstricted venules. From these data, we conclude that beta 2-adrenergic receptors are present in and mediate dilation of tracheal arterioles, and also, that the dilation in large tracheal venules is mediated in large part through beta 1-adrenergic receptors.
Corboz
M R
MR
College of Medicine, University of South Alabama, Mobile 36688, USA.
Ballard
S T
ST
Inglis
S K
SK
Taylor
A E
AE
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001160:Arterioles / Q000187:drug effects; D001262:Atenolol / Q000494:pharmacology; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D008833:Microcirculation / Q000187:drug effects; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D011943:Receptors, Adrenergic, beta / Q000187:drug effects*; D013726:Terbutaline / Q000494:pharmacology; D014132:Trachea / Q000098:blood supply* / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation; D014665:Vasodilator Agents / Q000494:pharmacology*; D014699:Venules / Q000187:drug effects; D014741:Video Recording
D000316:Adrenergic alpha-Agonists; D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D011943:Receptors, Adrenergic, beta; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D010656:Phenylephrine; D001262:Atenolol; D007545:Isoproterenol; D013726:Terbutaline