EFFECTS OF CALCIUM BUFFERS AND TEMPERATURE ON THE BETA-RECEPTOR-MEDIATED REGULATION OF THE SLOWLY ACTIVATING POTASSIUM CURRENT (I(KS) IN GUINEA-PIG CARDIAC MYOCYTES

The slowly activating potassium current, termed I(Ks) [1], was measured in guinea pig ventricular myocytes with the whole-cell patch clamp configuration. With low concentrations of Ca2+ buffer (0.1 mM EGTA or BAPTA) in the recording pipette, a temperature increase from 21 to 31-degrees-C dramatically accelerated activation of I(Ks). Isoproterenol increased I(Ks) under such conditions 2- to 3-fold at both temperatures. With high internal Ca buffer concentrations (EGTA or BAPTA greater-than-or-equal-to 10 mM), I(Ks) was regulated by isoproterenol at 31-degrees-C but not at 21-degrees-C. We conclude that beta-receptor regulation of I(Ks) is temperature and [Ca2+]i dependent. A mechanism consistent with the results is that Ca2+ and temperature increase the availability of subunits for channel formation and regulation by the beta-adrenergic pathway.