DISTRIBUTION OF FUNCTIONAL ADRENERGIC-RECEPTOR SUBTYPES IN THE MICROCIRCULATION OF RAT TRACHEA

Although blood flow to the pulmonary airways is known to be largely under sympathetic control, virtually nothing is known about adrenergic regulation of vascular segments within the airway microcirculation. To evaluate the distribution of functional adrenergic receptor subtypes in the microvessels of the large airways, the change in diameter of adventitial vessels in rat trachea was measured following suffusion with selective and nonselective receptor agonists and antagonists. Microvessels were viewed with a video microscope, and vessel diameters were measured using video calipers. Arterioles (11.0 to 40.0 mu m, n = 32), small postcapillary venules (11.0 to 26.0 mu m, n = 16), medium venules (28.0 to 59.5 mu m, n = 40), and large collecting venules (61.0 to 99.0 mu m, n = 42) were distinguished. Similar sensitivities to norepinephrine (NE), a mixed alpha(1) and alpha(2) agonist, were observed in arterioles and medium venules with EC(50) (agonist concentration needed to produce 50% of the maximal response) for contraction of 2.4 x 10(-7) and 3.3 x 10(-7) M, respectively. Large venules (EC(50) of 1.6 x 10(-6) M) were significantly (p < 0.05) less sensitive than arterioles to NE. In the presence of propranolol, a beta receptor antagonist, the EC(50) values for NE were not different between the three vessel groups, although the response to low doses of NE was significantly increased in arterioles. When vessels were treated with propranolol and phenylephrine, a selective alpha(1) agonist, arterioles (EC(50) of 4.1 x 10(-7) M) were significantly more sensitive than large venules (EC(50) of 4.9 x 10(-6) M). Prazosin, an alpha(1)-adrenergic receptor antagonist, caused a significant rightward shift in the concentration-response curve to NE in presence of propranolol, suggesting that alpha(1) adrenoceptors mediated the constrictor response. Although poorly responsive to all agonists, small postcapillary venules exhibited the greatest constrictor response when pretreated with propranolol and prazosin. From these data, we conclude that (i) alpha(1) receptors are present and mediate constriction in all tracheal vessels except small venules, (ii) beta receptors oppose constriction in arterioles and large venules, and (iii) alpha(2) receptors may facilitate constriction of the small postcapillary venules.