Am. J. Respir. Crit. Care Med., Vol 153, No. 3, 03 1996, 1093-1097.
Tracheal microvascular responses to beta-adrenergic stimulation in anesthetized rats
MR Corboz, ST Ballard, SK Inglis and AE Taylor
College of Medicine, University of South Alabama, Mobile 36688, USA.
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.
