AJP - Gastrointestinal and Liver Physiology, Vol 271, Issue 1 27-G35, Copyright © 1996 by American Physiological Society
Nitric oxide attenuates endothelin-1-induced vasoconstriction in canine stomach
J. G. Wood, Q. Zhang, Z. Y. Yan and L. Y. Cheung
Department of Surgery, University of Kansas Medical Center, Kansas City 66160, USA.
We previously observed that endothelin-1 (ET-1)-induced gastric
vasoconstriction is enhanced after ischemia-reperfusion. The purpose of our
present study was to examine the role of nitric oxide in regulating
ET-1-induced vasoconstriction under normal conditions and after
ischemia-reperfusion. Using a mechanically perfused stomach segment from
chloralose-anesthetized dogs, we examined 1) responses to
NG-nitro-L-arginine methyl ester (L-NAME) alone and in combination with
L-arginine, 2) whether L-NAME affects ET-1-induced vasoconstriction under
normal conditions and after ischemia-reperfusion, and 3) if spermine
NONOate inverted question
mark1,3-propanediamine-N-[4-1-(3-aminopropyl)-2-hydroxy-2-nitrosohydrazi
no] butyl; a nitric oxide donor inverted question mark attenuates the
augmented response to ET-1 after 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
ischemia-reperfusion. Our findings are consistent with the hypothesis that
nitric oxide modulates responses to ET-1 under normal conditions, and loss
of this vasodilator after ischemia-reperfusion results in an augmented
response to ET-1.
