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

1998; American Physiological Society; Volume: 274; Issue: 1 Linguagem: Inglês

10.1152/ajpgi.1998.274.1.g170

1522-1547

Ágnes Király, Gábor Sütő, Paul H. Guth, Yvette Taché,

Nitric Oxide and Endothelin Effects

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 H 1 receptor antagonist pyrilamine (intravenously), capsaicin (subcutaneously, −10 days), and N G -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 N G -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 thel-NAME effect was reversed by intravenous l- but notd-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 stimulatingl-arginine-nitric oxide pathways, whereas H 1 receptors and capsaicin-sensitive afferent fibers do not play a role.