The effect of different calcium antagonists on histamine-and carbachol-induced acid secretion in the isolated mouse stomach
- 16 Downloads
Earlier experiments suggested that the action of muscarinic agonists in gastric acid secretion might be partly mediated by endogenous histamine release. This possibility could be tested by use of various calcium antagonists provided that they show different activity on histamine- and carbachol-induced secretion.
In the present work, three calcium antagonists, verapamil, nifedipine, and sodium nitroprusside were used on the isolated mouse stomach where acid secretion induced by histamine and by carbachol was measured.
Verapamil (100 μM) did not affect either histamine or carbachol-induced acid secretion. Nifedipine (100 μM) reduced histamine-induced acid secretion, whereas the effect of carbachol remained unchanged. Sodium nitroprusside (10–100 μM) reduced both histamine- and carbachol-induced acid secretion.
The differences in action of calcium antagonists in histamine- and carbachol-induced acid secretion could exclude the possibility that the effect of carbachol is partly mediated by histamine release from mast cells present in the mouse stomach.
KeywordsMast Cell Histamine Verapamil Nifedipine Gastric Acid
Unable to display preview. Download preview PDF.
- L. Stanovnik and F. Erjavec,Histamine in gastric secretion—a study on the isolated mouse stomach. Iugoslav. Physiol. Pharmacol. ActaSuppl. 2, 218–220 (1983).Google Scholar
- R. Raddino, E. Poli, R. Ferrari and O. Visioli,Effects of calcium entry blockers not connected with calcium channels inhibition. Gen. Pharmac.18, 431–436 (1987).Google Scholar
- R. Brage, J. Cortijo, J. V. Esplugues, E. Marti-Bonmati and C. Rodrigues,Effects of calcium channel blockers on gastric emptying and acid secretion of the rat in vivo. Br. J. Pharmac.89, 627–633 (1986).Google Scholar
- N. Chand, W. Diamantis, J. Pillar and R. D. Sofia,Inhibition of allergic and non-allergic histamine secretion from rat peritoneal mast cells by calcium antagonists. Br. J. Pharmac.83, 899–902 (1984).Google Scholar