Abstract

In isolated and cross-circulated canine A–V node preparations single injections of Mn 2+ (1–30 μmol) and verapamil (0.3–10 nmol) into the posterior septal artery (PSA) caused a dose-dependent increase in the A–V conduction time and, in large doses, produced A–V conduction block. The A–V conduction time increased by Mn 2+ and verapamil is restored by 1-norepinephrine (1-NE) injected into the PSA. The A–V nodal tachycardia induced by 1-NE is suppressed by Mn 2+ but not by verapamil. These indicate the following: (1) the slow Ca 2+ channel plays an important role in A–V conduction; (2) the positive dromotropic response of the A–V node to 1-NE may have some relations to the Ca 2+ channel; (3) the A–V nodal tachycardia induced by 1-NE may be mediated by the Ca 2+ channel. Possible causes which produced differences between Mn 2+ and verapamil in the effects in antagonizing the 1-NE-induced A–V nodal tachycardia are discussed.

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