Abstract
IN heart cells, the catecholamine-activated cyclic AMP system regulates calcium1 and potassium2–4 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 airway5–9 and colonic10,11 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 cells10,11. This channel could be responsible for the β-catecholamine-induced increase in cardiac membrane conductance12 that has been attributed to activation of a Cl− current13–15. 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.
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Ehara, T., Ishihara, K. Anion channels activated by adrenaline in cardiac myocytes. Nature 347, 284–286 (1990). https://doi.org/10.1038/347284a0
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DOI: https://doi.org/10.1038/347284a0
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