Vol. 277, Issue 4, H1441-H1446, October 1999
NO mediates postjunctional inhibitory effect of neurogenic ACh
in guinea pig small intestinal microcirculation
N.
Kotecha and
F. P.
Coffa
Department of Physiology, Monash University, Clayton, Victoria 3168, Australia
The present
study was designed to evaluate the role of the endothelium as an
effector organ of neurally mediated inhibition of vascular tone.
Acetylcholine (ACh), either released by stimulation of the submucosal
ganglia or applied exogenously, inhibited phenylephrine (PE)-induced
constrictions in arterioles of the guinea pig intestinal submucosa.
NG-monomethyl-L-arginine
(L-NMMA), an inhibitor of nitric
oxide (NO) synthesis, attenuated the response to superfused ACh by 74% compared with 94% attenuation obtained with
NG-nitro-L-arginine
(L-NNA).
L-NNA attenuated the
response to neurally released ACh by 98% and that to iontophoretically
applied ACh by 92%. L-Arginine reversed the effects of
both L-NMMA and
L-NNA. Functional integrity of
the endothelium was essential for the neurally mediated inhibition of
PE-induced constrictions. However, neurogenic inhibition of neurally
evoked constrictions was preserved despite endothelial disruption. It
was concluded that at the postjunctional level, the mechanism of action
of neurally released ACh was almost exclusively via a NO-dependent
pathway, with the source of NO being the vascular endothelium.
submucosal arterioles; vasodilator nerves; acetylcholine; endothelium
