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 a subunit of PTX-sensitive G proteins activates the K(ATP) channels, while betagamma subunits activate the K(ACH) channel. The physiologic significance of this heterogeneous mechanism remains to be determined.