Summary
The effects of two “specific bradycardic agents“, falipamil (AQ-A 39) and the alinidine-congener STH 2148 2-[N-(cyclopropylmethyl)-N-(2,6-dibromophenyl)amino]2-imidazoline, on the spontaneous electrical discharge rate of intact guinea-pig sinus node preparations were investigated in comparison to that of the “calcium channel blocker” verapamil. Addition of falipamil (10 μg/ml) to a maximally rate lowering concentration of STH 2148 (30 μg/ml) exerted no further bradycardic effect. In contrast, verapamil (0.1 μg/ml) added to either STH 2148 (30 gg/ml) or a maximally effective concentration of falipamil (30 gg/ml) resulted in a further, significant reduction of sinus rate. The results are compatible with the idea of a common mechanism of the two specific bradycardic agents, different from that of calcium channel blockers.
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Lillie, C., Kobinger, W. Investigations differentiating the mechanism of specific bradycardic agents from that of calcium channel blockers. Naunyn-Schmiedeberg's Arch Pharmacol 335, 331–333 (1987). https://doi.org/10.1007/BF00172806
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DOI: https://doi.org/10.1007/BF00172806