Blockade of the Ca²⁺-dependent Bioelectrical Automaticity and Electromechanical Coupling of Smooth Muscle Cells by Gallopamil (D 600)

Abstract

Like mechanical tension development in myocardial fibres, the contractile activation of smooth muscle cells is a function of Ca²⁺ ions. Naturally, therefore, withdrawing Ca²⁺ also results in a failure of the Ca²⁺-dependent electromechanical coupling reactions and hence in a loss of tonic and phasic contractility in the smooth musculature too (Bohr 1964; Bozler 1962; Rüegg 1971; Schatzmann 1964; Somlyo and Somlyo 1968, 1970; Weiss 1977). Furthermore, in smooth muscle cells the electrogenesis of spike potentials is also associated with a transmembrane influx of Ca²⁺ ions as electrical charge carriers (for detailed review of the literature see Fleckenstein 1983). However, unlike the skeletal musculature and myocardium, here the influx of Na⁺ ions only appears to play a subordinate role in the generation of action potentials. Accordingly, smooth muscle cells also have no tetrodotoxin (TTX)-sensitive Na⁺ carrier system. At all events, apart from abolishing the contractility of smooth muscle fibres, withdrawing Ca²⁺ also normally abolishes their bioelectrical activity. Thus, for the experimental testing of Ca²⁺ antagonists on smooth musculature, two aims were stipulated at the outset:

• 1. To analyse the effects of Ca²⁺ antagonists on the Ca²⁺-dependent excitation processes.

• 2. To study the effects of Ca²⁺ antagonists on the Ca²⁺-dependent electromechanical coupling reactions.