Acetylcholine induces conducted vasodilation by nitric oxide
-dependent and -independent mechanisms.
Doyle, Michael P., and Brian R. Duling.
Department of Molecular Physiology and Biological Physics,
University of Virginia Health Sciences Center, Charlottesville, VA
22908
APStracts 3:0441H, 1996.
Conducted vasodilation has been proposed as an important component of
local vascular control. Because conducted vasomotor responses have
previously been studied only in response to short pulses (<
500 ms) of agonist, this study examined conducted vasodilation in
response to sustained stimuli. In addition, we examined the
contribution of nitric oxide to initiation and maintenance of
conducted responses induced by acetylcholine (ACh). Responses to 2
min applications of ACh, sodium nitroprusside (SNP), and 8-Br-cGMP
were obtained in cannulated, perfused hamster cheek pouch arterioles
(approximately 60 [mu]m in diameter). Changes of luminal diameter in
response to pressure ejection of agonists from a micropipette placed
close to the downstream end of the vessel were observed at the site
of stimulation ("local") as well as 570 and 1140 [mu]m
upstream. At the local site, ACh stimuli produced large changes in
diameter (approximately 70% of the maximum response) that peaked
within 45 s before declining slowly to levels of approximately 50% of
the maximum response. A similar response pattern was observed at both
upstream sites with the conducted responses being maintained for the
duration of the stimulus. Local responses of similar magnitude were
found with SNP and 8-Br-cGMP, but only minimal responses were
observed at the conducted sites. In a separate set of arterioles, ACh
responses were obtained before and during perfusion with 10 [mu]M Nw
-nitro-L-arginine (L-NAME). Inhibition of nitric oxide synthesis
diminished the local response to ACh, but the initial phase of the
conducted response was unaffected. Furthermore, the conducted
responses faded more rapidly in the presence of L-NAME. We conclude
from these results that local NO synthesis alone is insufficient to
initiate conducted responses but that NO synthesis contributes to
maintenance of sustained conducted responses.
Received 7 March 1995; accepted in final form 30 September 1996.
APS Manuscript Number H214-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996