Am. J. Respir. Crit. Care Med., Vol 154, No. 5, Nov 1996, 1382-1386.
Tracheal microvascular responses to inhibition of nitric oxide synthesis in anesthetized rats
MR Corboz, ST Ballard, SK Inglis and AE Taylor
Department of Physiology, College of Medicine, University of South Alabama, Mobile, USA.
We previously demonstrated that rat tracheal arterioles and large venules
constrict in response to alpha-adrenergic agonists and dilate in response
to beta-adrenergic agonists. To further investigate the vasodilatory
mechanisms in these vessels, we hypothesized that the vascular tone in the
tracheal microcirculation is regulated in part by endogenously released
nitric oxide (NO). To test this hypothesis, rat tracheal microvessels were
visualized in vivo with a video microscope. The change in diameter af
adventitial arteriolar (14.5 to 42.0 microm initial diameter, n = 41) and
large venular (50.0 to 100.0 microm initial diameter, n = 41) microvessels
following the suffusion of vasoactive drugs was measured with video
calipers. Significant constriction was observed in arterioles (to 70.0% of
initial diameter) and large venules (to 76.6% of initial diameter) after 20
min of suffusion with L-NAME, an inhibitor of NO synthesis. This
constriction was in large part reversed by L-arginine, a biochemical
precursor of NO, in arterioles (to 93.2% of initial diameter) and in
venules (to 90.8% of initial diameter). The combination of prazosin, a
selective alpha1-adrenergic antagonist, and yohimbine, a selective alpha2-
adrenergic antagonist, also reduced L-NAME-induced constriction in
arterioles (to 87.9% of initial diameter) and in venules (to 85.2% of
initial diameter). L-arginine or the combination of prazosin and yohimbine
alone did not affect the diameter of tracheal microvessels. These data
suggest that NO exerts an important influence on tracheal microvascular
tone in rats, and may attenuate alpha-adrenergic constriction in these
vessels.
