抄録
The role of histamine H2-receptors in AV nodal conduction was estimated in the blood-perfused AV node preparation of the dog. Histamine injected into the AV node artery caused an initial, predominant, dose-related prolongation of the AH interval, which was followed by a slight but significant shortening. Diphenhydramine, an H1-antagonist, abolished the initial prolongation, but the shortening was slightly enhanced. Cimetidine, an H2-antagonist, abolished the shortening and potentiated the initial prolongation. Dimaprit, an H2-agonist, caused only a slight, dose-related shortening of the AH interval, which was abolished by cimetidine. The shortening induced by either histamine or dimaprit was slightly suppressed, but was never abolished by atenolol, a beta-blocker, which completely abolished the noradrenaline-induced shortening. These results indicate that a positive dromotropic effect via H2-receptors exists in the canine AV node, although the main effect of histamine on AV nodal conduction is a negative one via H1-receptors.
