Gastric hyperemic and acid responses to the stable thyrotropin-releasing hormone (TRH) analog RX-77368 injected intracisternally at a cytoprotective dose were investigated, as well as the underlying mechanisms of the responses. Gastric acid secretion (GAS), mucosal blood flow (GMBF; measured by the hydrogen gas clearance technique), and mucosal vascular resistance (GMVR) and mean arterial pressure (MAP) were assessed simultaneously for 30 min before and after RX-77368 (1.5 ng) administration in urethan-anesthetized rats. RX-77368 increased GMBF from 46.8 ± 5.3 to 100.6 ± 20.9 ml · min- 1 · 100 g-1 and MAP from 70.3 ± 2.1 to 84.3 ± 5.9 mmHg and decreased GMVR from 1.50 ± 0.33 to 0.84 ± 0.08 mmHg · ml-1 · min · 100 g, whereas GAS was not significantly altered (1.8 ± 0.4 vs. 4.7 ± 1.7 μmol/30 min) in vehicle-pretreated rats. The GMBF, MAP, and GMVR responses to RX- 77368 were not modified by indomethacin (5 mg/kg ip), whereas GAS was increased. In rats pretreated with capsaicin (125 mg/kg sc) or calcitonin gene-related peptide (CGRP) antagonist hCGRP-(8-37), intracisternal RX-77368 did not increase GMBF or decrease GMVR but did stimulate GAS. These data show that vagal stimulation by the TRH analog RX-77368 injected intracisternally at a nonacid secretory dose increases GMBF. Gastric hyperemia is mediated by CGRP contained in capsaicin-sensitive afferent fibers, whereas acid secretion is under the inhibitory influence of prostaglandins and CGRP.
|Journal||American Journal of Physiology - Gastrointestinal and Liver Physiology|
|Issue number||1 36-1|
|Publication status||Published - Jul 1997|
- Calcitonin gene-related peptide antagonist
- Gastric mucosal blood flow
ASJC Scopus subject areas
- Physiology (medical)