Anion channels activated by adrenaline in cardiac myocytes

Abstract

IN heart cells, the catecholamine-activated cyclic AMP system regulates calcium¹ and potassium^2–4 channels. We report here a novel class of chloride channels that can be activated by adrenaline in mammalian ventricular cells. Like the agonist-activated ^Cl− channel currents of airway^5–9 and colonic^10,11 epithelial cells, the cardiac CF-channel current shows outward rectification. But the unit conductance of cardiac Cl⁻ channels is smaller than that of epithelial Cl⁻ channels. The cardiac ^Cl− channel is functionally voltage-independent, in contrast to the Cl⁻ channel in colonic epithelial cells^10,11. This channel could be responsible for the β-catecholamine-induced increase in cardiac membrane conductance¹² that has been attributed to activation of a Cl⁻ current^13–15. Thus, sympathetic control of cardiac electrical activity involves not only the voltage-dependent, excitation-related cation channels, but also anion channels that generate a steady current.