G-protein control of cardiac potassium channels.
Two cardiac potassium (K(+)) channels are activated by pertussis toxin (PTX)-sensitive G proteins either directly or in a "membrane-delimited" manner. They are muscarinic K(+)(K(ACH)) and ATP-sensitive K(+)(K(ATP)) channels. K(ACH) channels are responsible for acetylcholine (ACh)- or adenosine-induced deceleration of the heartbeat and atrioventricular conduction, while K(ATP) channels are responsible for the ischemia-induced shortening of the cardiac action potential and possibly for the adenosine-mediated protection from ischemic damage. Distinct molecular mechanisms underlie G-protein activation of these cardiac K(+) channels; the α subunit of PTX-sensitive G proteins activates the K(ATP) channels, while βγ subunits activate the K(ACh) channel. The physiologic significance of this heterogeneous mechanism remains to be determined.
Division of Cardiovascular Diseases, Department of Internal Medicine and Department of Pharmacology, Mayo Clinic, Rochester, MN 55905, USA; Department of Pharmacology II, Osaka University School of Medicine, Siuta, Osaka 565, Japan.
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Kurachi