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Asocainol, a new antiarrhythmic drug with natrium- and calcium-antagonistic effects on ventricular myocardium.

In isolated guinea pig papillary muscles, asocainol, a new antiarrhythmic drug, and its optical isomers exert a concentration-dependent negative inotropic action that is due to an inhibitory influence on the slow Ca2+ influx. However, depression of contractility is always accompanied by marked alterations of normal Na+-carried action potentials; thus, overshoot and duration decline together with Na+-dependent upstroke velocity. These observations indicate that asocainol not only inhibits Ca2+ inflow, but interferes with the fast inward Na+ current. In partially depolarized ventricular muscle, asocainol lowers Ca2+-dependent contractile force as it reduces upstroke velocity, overshoot, and duration of Ca2+-mediated action potentials. Moreover, Mg2+-induced membrane activity is suppressed by asocainol. Ba2+-induced ventricular autorhythmicity, representing a model of a slow-channel-dependent ectopic pacemaker, is abolished by asocainol. We conclude that asocainol exerts mixed Na+-, Ca2+-, and Mg2+-antagonistic effects in mammalian ventricular myocardium. Thus, asocainol keeps an intermediate position between specific Ca2+ antagonists (verapamil) and predominantly Na+-antagonistic drugs such as certain local anesthetics. On the basis of this dual inhibitory action on both transmembrane Na+ and Ca2+ conductivities, it is easily understood that asocainol is a rather efficient antiarrhythmic agent that exerts in combination the particular effects of both class-I and class-IV antiarrhythmic drugs.

Action Potentials↗
PubMed1984

[Pharmacological characteristics of the acetylcholine and L-glutamate receptors of the subpharyngeal ganglion neuron in the mollusk Zachrysia guanensis].

The presence of acetylcholine and L-glutamate receptors sensitive to the cholinoreceptor-specific ligands cytizine and tubocurarine has been demonstrated by means of microapplication of acetylcholine and L-glutamate to the central parietal zone of the subpharyngeal ganglion of the mollusc Zachrysia guanensis. Azidocytizine inhibited the function of acetylcholine receptor but did not affect glutamate receptor. Based on the electrophysiological data and analysis of ligand conformations a model has been designed for a site where L-glutamine is recognized by glutamine receptor.

Acetylcholine↗