The effect and mechanism of action of capsaicin on gastric acid output.
BACKGROUND
Capsaicin has beneficial pharmacological properties, such as the ability to improve appetite and digestion. However, capsaicin has been reported to suppress gastric acid output, but to increase secretion; no consensus as to its effects on gastric acid output has been reached, and the underlying mechanisms remain to be elucidated.


METHODS
Rat gastric lumen was perfused with capsaicin. Basal acid output and gastric acid secretion stimulated by vagal nerve activation and bethanecol, a muscarinic receptor agonist, were measured. After intravenous infusion of calcitonin gene-related peptide (CGRP), the measurements were repeated. The secretion of gastrin, somatostatin, and histamine was measured in isolated vascularly perfused rat stomach after vagal nerve and bethanecol stimulation, and under the influence of capsaicin.


RESULTS
Capsaicin administration had no effect on basal gastric acid output, but inhibited acid secretion resulting from vagal stimulation. Capsaicin had no effect on acid secretion resulting from stimulation with bethanecol. Administration of high-dose CGRP inhibited basal acid output and gastric acid secretion from both vagal nerve and bethanecol stimulation. Low-dose CGRP inhibited gastric acid secretion because of vagal stimulation, but had no effect on basal secretion or acid secretion following stimulation with bethanecol. Capsaicin administration inhibited the stimulated gastrin and histamine secretion and reversed the suppression of somatostatin secretion mediated by vagal stimulation. However, capsaicin had no effect on stimulated gastrin secretion, suppression of somatostatin secretion, or stimulated histamine secretion because of bethanecol.


CONCLUSIONS
Capsaicin inhibited gastric acid output, and the mechanism underlying this effect appears to involve vagal nerve inactivation.
Imatake
Kazuhiro
K
Department of Medicine, Division of Gastroenterology and Hepatology, Nihon University School of Medicine, Tokyo, Japan. imatake@mbg.nifty.com
Matsui
Teruaki
T
Moriyama
Mitsuhiko
M
D000818:Animals; D001569:Benzodiazepines / Q000494:pharmacology; D018723:Bethanechol / Q000494:pharmacology; D015740:Calcitonin Gene-Related Peptide / Q000494:pharmacology; D002211:Capsaicin / Q000008:administration & dosage / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D015738:Famotidine / Q000494:pharmacology; D005744:Gastric Acid / Q000378:metabolism*; D005755:Gastrins / Q000378:metabolism; D006632:Histamine / Q000378:metabolism; D006635:Histamine H2 Antagonists / Q000494:pharmacology; D006727:Hormone Antagonists / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D018721:Muscarinic Agonists / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013004:Somatostatin / Q000378:metabolism; D013270:Stomach / Q000294:innervation; D014630:Vagus Nerve / Q000502:physiology
D005755:Gastrins; D006635:Histamine H2 Antagonists; D006727:Hormone Antagonists; D018721:Muscarinic Agonists; D018723:Bethanechol; D001569:Benzodiazepines; C087260:YM 022; D013004:Somatostatin; D015738:Famotidine; D006632:Histamine; D015740:Calcitonin Gene-Related Peptide; D002211:Capsaicin