Nitric oxide modulates arteriolar responses to increased
sympathetic nerve activity.
Nase, Geoffrey P., and Matthew A. Boegehold.
Department of Physiology, West Virginia University School of
Medicine, Morgantown, West Virginia 26506-9229
APStracts 3:0056H, 1996.
The purpose of this study was to determine if arteriolar responses to
increased sympathetic nerve activity are limited by the actions of
endogenous nitric oxide. Intravital microscopy was used to examine
diameter responses of small feed arteries (SFAs), first-order
arterioles (1As) and second-order arterioles (2As) to perivascular
sympathetic nerve stimulation in the superfused rat small intestine.
Stimulation induced a frequency-dependent constriction in all vessel
types that was completely abolished by the [alpha]-adrenoceptor
antagonist phentolamine (10-6 M). In SFA and 1A, the magnitude of
sympathetic constriction was increased significantly in the presence
of the nitric oxide synthase inhibitor NG-monomethyl L-arginine (L
-NMMA, 10-4 M). In SFAs (n=7), stimulation at 3, 8, and 16 Hz induced
constrictions of 11 +/- 1%, 28 +/- 4% and 42 +/- 3% respectively
under the normal superfusate vs 28 +/- 3%, 46 +/- 5% and 76 +/- 3% in
the presence of L-NMMA. For 1As (n=7), stimulation induced
constrictions of 10 +/- 1%, 27 +/- 4% and 37 +/- 3% under the normal
superfusate vs 24 +/- 2%, 47 +/- 3% and 72 +/- 4% in the presence of
L-NMMA. The effect of L-NMMA on sympathetic constriction in SFAs (n =
7) was completely reversed by the additional presence of 5 x 10-3 M
L-arginine in the superfusate. These results suggest that endogenous
nitric oxide activity can attenuate sympathetic neurogenic
constriction in the intestinal microvasculature.
Received 19 October 1995; accepted in final form 23 January 1996.
APS Manuscript Number H976-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 8 February 96