1Experiments were designed to evaluate the effects of three calcium channel blockers (verapamil, diltiazem and cinnarizine) on gastric emptying and secretion in the rat 2 Pretreatment with the calcium blockers delayed gastric emptying of phenol red in a dose-dependent manner. Verapamil was the most effective of the agents tested. 3 Verapamil and diltiazem inhibited gastric acid secretion in the pylorus-ligated rat without affecting pepsin output. Cinnarizine was ineffective in this model. 4 When the perfused lumen of the anaesthetized rat was used, verapamil was found to inhibit responses to carbachol or histamine more than those to pentagastrin. Further, we found a greater sensitivity to verapamil for basal compared with vagal-stimulated (2-deoxy-D-glucose) acid secretion. Neither diltiazem nor cinnarizine modified gastric acid secretion in this experimental model. 5 These findings are discussed in relation to the role of extracellular calcium in gastric motility and secretion, and the existence of a regional and functional selectivity for calcium blockers is proposed.

Verapamil (3, 10, 20 mg/kg^–1) increases the necrotizing effects of oral 25% NaCl or 100% ethanol. Damage by 0.6 N HCl was not equally affected since 1 mg/kg^–1 of verapamil decreased the ulcer index whereas the higher doses augmented it. Pharmacologically induced gastric lesions were also differently affected by verapamil, ulcers produced by histamine being greatly enhanced and those of reserpine inhibited. Neither indomethacin nor compound 48/80 ulcers were modified. These results suggest that verapamil modifies the susceptibility of the gastric mucosa to damage.