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G protein mediated regulation of K+ channels in heart.

Neuroendocrine control of cardiac function involves extensive regulation of potassium (K +) currents via specific receptors in various anatomical regions of the heart (22, 53, 54, 60). Recent evidence, to be considered here, indicates that these regulatory processes involve a relatively complex cascade in which receptor activation is coupled to channel opening by guanine nucleo­ tide binding proteins (G proteins). Of the various K+ channels in the heart (see, for example 60), the inwardly rectifying K+ current IK(AChl activated by muscarinic agonists or adenosine, the delayed rectifier IK, and the background K+ conductance gK are thought to be regulated via G proteins either directly or indirectly. The regulation of IK(AChl is of particular interest, not only because it has been the most thoroughly studied, but also because it represents a novel mechanism involving the direct activation of a channel by a receptor-linked G protein. Moreover, IK(AChl serves as a rapid, sensitive and specific indicator of G protein function that may be used to explore with unprecedented time resolution the receptor-G protein interactions that underlie a large number of neuroendocrine responses.