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+ (I(K)) channels in guinea-pig sinoatrial node (SAN) and compare SAN I(K) to the better characterized ventricular I(K). Despite demonstrated similarities in the properties of I(K) in guinea-pig ventricle and SAN, the possibility remains that expression of I(K) channels can vary regionally within the same heart. Like ventricular I(K), SAN I(K) can be enhanced by beta-adrenergic stimulation and exposure to phorbol ester. However, in contrast to ventricular I(K), regulation of SAN I(K) by protein kinases A and C is not temperature dependent. Basal SAN I(K) can be diminished by muscarinic agonists, while beta-adrenergic stimulation is a precondition for reduction of ventricular I(K) 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 I(K). The corresponding single-channel conductance of 6 pS is somewhat larger than that estimated for ventricular I(K) Overall comparisons of guinea-pig ventricular and SAN I(K) to the current associated with the minK channel clone suggest that the native guinea-pig cardiac I(K) channels may be related not only to each other but also to the minK channel protein.