Nitric oxide attenuates endothelin-1-induced vasoconstriction in
the canine stomach.
Wood, J. G., Q. Zhang, Z. Y. Yan, and L. Y. Cheung.
Departments of Surgery and Physiology, University of Kansas Medical
Center, Kansas City, KS 66160
APStracts 2:0235G, 1995.
We previously observed that endothelin-1-(ET-1)-induced gastric
vasoconstriction is enhanced following ischemia/reperfusi on. The
purpose of our present study was to examine the role of nitric oxide
in regulating ET-1-induced vasoconstriction under normal conditions
and following ischemia/reperfusion. Using a mechanically-perfused
stomach segment from chloralose-anesthetized dogs, we examined: 1)
responses to L-NAME alone and in combination with L-arginine, 2)
whether L-NAME affects ET-1-induced vasocon striction under normal
conditions and after ischemia/reperfusion, and 3) if spermine NONOate
(a nitric oxide donor) attenuates the augmented response to ET-1
following ischemia/reperfusion. Our results show that: 1) L-NAME
significantly increased baseline vascular resistance and this
response was reduced by L-arginine, 2) ET-1-induced vasoconstriction
was enhanced by L-NAME, and 3) administration of spermine NONOate
during reperfusion largely attenuated the vasoconstrictor response to
ET-1 after is chemia/reperfusion. Our findings are consistent with
the hypothe sis that nitric oxide modulates responses to ET-1 under
normal conditions, and loss of this vasodilator following isch
emia/reperfusion results in an augmented response to ET-1.
Received 12 January 1995; accepted in final form 3 November 1995.
APS Manuscript Number G17-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 November 95