G-protein control of cardiac potassium channels

Trends Cardiovasc Med. Mar-Apr 1994;4(2):64-9. doi: 10.1016/1050-1738(94)90011-6.

Abstract

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.