Delayed rectifier potassium channels in ventricle and sinoatrial node of the guinea pig: molecular and regulatory properties.

We focus on the regulatory properties of delayed rectifier K+ (IK) channels in guinea-pig sinoatrial node (SAN) and compare SAN IK to the better characterized ventricular IK. Despite demonstrated similarities in the properties of IK in guinea-pig ventricle and SAN, the possibility remains that expression of IK channels can vary regionally within the same heart. Like ventricular IK, SAN IK can be enhanced by beta-adrenergic stimulation and exposure to phorbol ester. However, in contrast to ventricular IK, regulation of SAN IK by protein kinases A and C is not temperature dependent. Basal SAN IK can be diminished by muscarinic agonists, while beta-adrenergic stimulation is a precondition for reduction of ventricular IK by cholinergic agonists. Nonstationary state fluctuation analysis predicts a small single-channel current (1 pA) and a large number of functional channels (308) associated with whole-cell SAN IK. The corresponding single-channel conductance of 6 pS is somewhat larger than that estimated for ventricular IK. Overall comparisons of guinea-pig ventricular and SAN IK to the current associated with the minK channel clone suggest that the native guinea-pig cardiac IK channels may be related not only to each other but lso to the minK channel protein.