Central vagal activation by TRH induces gastric hyperemia: role of CGRP in capsaicin-sensitive afferents in rats
Kiràly, A.; Sütö, G.; Livingston, E.H.; Guth, P.H.; St Pierre, S.; Taché, Y.
American Journal of Physiology 267(6 Pt 1): G1041-G1049
1994
ISSN/ISBN: 0002-9513 PMID: 7810651 Document Number: 433220
The role of calcitonin gene-related peptide (CGRP) in the vagal cholinergic-mediated increase in gastric mucosal blood flow (GMBF) induced by the stable thyrotropin-releasing hormone (TRH) analogue RX77368 injected intracisternally (ic, 30 ng) was investigated in urethan-anesthetized rats using the hydrogen gas clearance technique. alpha-CGRP (14 mu-g cntdot kg-1 cntdot h-1) or bethanechol (150 mu-g cntdot kg-1 cntdot h-1) infused close intra-arterially to the stomach or RX-77368 injected intracisternally increased GMBF by 76, 102, and 131%, respectively, 30 min after administration. The CGRP antagonist, human CGRP-(8-37) (hCGRP-(8-37)), injected intravenously (15 pg/kg bolus and 3 mu-g cntdot kg-1 cntdot h-1) inhibited by 100, 97, and 73% the gastric hyperemic response to alpha-CGRP, TRH analogue, and bethanechol, respectively, whereas the substance P antagonist CP-96,345 (3 mg/kg iv) had no effect. In capsaicin-pretreated rats, hCGRP-(8-37) no longer blocked the increase in GMBF induced by intracisternal RX-77368. These results suggest that the gastric hyperemic response to central vagal activation induced by intracisternal TRH analogue at 30 ng is mediated by local effector function of capsaicin-sensitive afferent fibers releasing CGRP.