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Am J Physiol Gastrointest Liver Physiol 274: G170-G177, 1998;
0193-1857/98 $5.00
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Vol. 274, Issue 1, G170-G177, January 1998

Peripheral mediators involved in gastric hyperemia to vagal activation by central TRH analog in rats

Ágnes Király, Gábor Sütö, Paul H. Guth, and Yvette Taché

Center for Ulcer Research and Education, Digestive Diseases Research Center, West Los Angeles Veterans Affairs Medical Center, and Department of Medicine and Brain Research Institute, University of California, Los Angeles, California 90073

Mechanisms mediating the increase in gastric mucosal blood flow (GMBF) induced by the stable thyrotropin-releasing hormone (TRH) analog RX-77368 injected intracisternally at a gastric acid secretory dose (30 ng) were investigated using hydrogen gas clearance in urethan-anesthetized rats. The histamine H1 receptor antagonist pyrilamine (intravenously), capsaicin (subcutaneously, -10 days), and NG-nitro-L-arginine methyl ester (L-NAME, intracisternally) failed to impair the 150% rise in GMBF induced by intracisternal injection of RX-77368. By contrast, atropine (subcutaneously) and NG-monomethyl-L-arginine (intravenously) completely inhibited the increase in GMBF evoked by intracisternal RX-77368. L-NAME (intravenously) blocked the intracisternal RX-77368-induced increase in GMBF in capsaicin-pretreated rats, and the L-NAME effect was reversed by intravenous L- but not D-arginine. These findings indicate that vagal efferent activation induced by TRH analog injected intracisternally at a gastric acid secretory dose increases GMBF through atropine-sensitive mechanisms stimulating L-arginine-nitric oxide pathways, whereas H1 receptors and capsaicin-sensitive afferent fibers do not play a role.

nitric oxide; atropine; histamine; capsaicin; NG-nitro-L-arginine methyl ester; thyrotropin-releasing hormone; blood pressure; acetylcholine; NG-monomethyl-L-arginine; pyrilamine; gastric vascular resistance


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