2 COMPONENTS OF[CA2-ACTIVATED CL- CURRENT DURING LARGE [CA2+](I) TRANSIENTS IN SINGLE-RABBIT HEART PURKINJE-CELLS(](I))

1. Single Purkinje cells, enzymatically isolated from rabbit ventricle , were studied under whole-cell voltage clamp conditions and internall y perfused with the fluorescent Ca2+ indicator fura-2 (100 mu M). 2. C a2+ release from the sarcoplasmic reticulum was either induced by exte rnal application of caffeine or occurred spontaneously in Ca-i(2+)-ove rloaded cells. Membrane currents accompanying these Ca2+-release signa ls were studied at steady membrane potentials. 3. [Ca2+](i) transients were accompanied by transient membrane currents. In the absence of Na +-Ca2+ exchange, two current components could be observed. The first c omponent peaked well before the [Ca2+](i) transient (I-fast) and relax ed before peak [Ca2+](i). The second component, on the other hand, pea ked at the time when [Ca2+](i) was maximal (I-slow). 4. In symmetrical Cl- solutions both current components had a reversal potential close to 0 mV. A reduction of external or internal [Cl-] shifted this revers al potential in accordance with the change of the Cl- equilibrium pote ntial. 5. Each [Ca2+](i) transient was accompanied by I-fast. Properti es of I-fast suggest that this current component is the [Ca2+](i)-depe ndent Cl- current, I-Cl(Ca), previously observed during depolarizing p ulses. 6. I-slow was only detected in cells that displayed a large [Ca 2+](i) transient with or without elevated resting [Ca2+](i). 7. It is concluded that during large [Ca2+](i) transients a low component of I- Cl(Ca) can be activated. This second component may arise from the same channel population as the previously described fast component and be related to the presence of spatial and temporal inhomogeneities of [Ca 2+](i). Alternatively, this current component may arise from a differe nt Cl- channel population with a different Ca2+ sensitivity.