Anion channels activated by adrenaline in cardiac myocytes.
In heart cells, the catecholamine-activated cyclic AMP system regulates calcium and potassium 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 and colonic epithelial cells, the cardiac Cl(-)-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. This channel could be responsible for the beta-catecholamine-induced increase in cardiac membrane conductance that has been attributed to activation of a Cl- current. 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.
Ehara
T
T
Department of Physiology, Saga Medical School, Japan.
Ishihara
K
K
D000818:Animals; D003994:Bucladesine / Q000494:pharmacology; D015220:Calcium Channels / Q000502:physiology*; D002462:Cell Membrane / Q000502:physiology; D004553:Electric Conductivity; D004837:Epinephrine / Q000494:pharmacology*; D006168:Guinea Pigs; D006321:Heart / Q000502:physiology*; D007700:Kinetics; D008564:Membrane Potentials; D009566:Nitrates / Q000494:pharmacology; D009994:Osmolar Concentration; D012965:Sodium Chloride / Q000494:pharmacology
D015220:Calcium Channels; D009566:Nitrates; D012965:Sodium Chloride; D003994:Bucladesine; C031618:sodium nitrate; D004837:Epinephrine