Abstract
The direct effects of famotidine, a selective histamine H2 receptor antagonist, on the cardiac repolarization process were assessed using two in vitro test systems. Neither famotidine (0.1 and 1 µM), nor its solvent, dimethylsulfoxide (0.1%), affected any of the action potential parameters of guinea-pig papillary muscles, whereas the positive control, dl-sotalol (30 µM), significantly prolonged the action potential duration. Moreover, neither famotidine (0.1, 1 and 10 µM) nor dimethylsulfoxide affected the human ether-a-go-go-related gene (hERG) K+ current expressed in Chinese hamster ovary-K1 cells, whereas the positive control, E-4031 (0.1 µM), significantly decreased the current. These results indicate famotidine does not directly affect the cardiac repolarization process.
