Effects of Isoproterenol, dl-Propranolol and d-Propranolol on the A-V Transmission and the A-V Nodal Transmembrane Action Potential

The A-V nodal transmembrane action potential was recorded along with contiguous bipolar electrograms from the right atrium and ventricle in 61 isolated rabbit hearts driven from a point near the S-A node at a constant frequency.Both dl- and d-propranolol prolonged the atrioventricular conduction time equally and this prolongation occurred not only in the anterior half of the A-V node but also in the ventricular conduction system. Isoproterenol shortened the atrioventricular conduction time. This shortening occurred mostly in the anterior half of the A-V node, and it was antagonized by dl-propranolol but not by d-propranolol.These findings suggest the following: (i) the negative dromotropic action of β-adrenergic blocking agents is mainly due to non-specific mechanisms in the isolated heart where catecholamines are insufficient, while in the sympathomimetic amine excess (isoproterenol administration) heart it is mainly due to β-blocking mechanisms: (ii) the dromotropic action mediated by β-adrenergic receptors occurs mostly in the anterior half of the A-V node.The second degree A-V block induced by either dl- or d-propranolol occurred between AN and N layer of the A-V node, and it always began with the Wenckebach phenomenon.The depolarization phase of the A-V nodal transmembrane action potential was shortened by isoproterenol, but prolonged by dl- and d-propranolol. These changes tended to be more marked in AN and N rather than NH layer. Above findings were considered to correspond to the dromotropic actions induced by these drugs.The slope of a slow diastolic depolarization recognized in only one A-V nodal fiber was increased by isoproterenol, but decreased by dl-propranolol.