Ca 2+ -activated K + currents (I K(Ca) ) can contribute to action potential repolarization and after-hyperpolarization in GH 3 cells. In this study, we examined how the activation of I K(Ca) at the cellular level could be functionally coupled to Ca 2+ influx through L-type Ca 2+ channels. A 30-msec Ca 2+ influx step to 0 mV was found to exhibit substantial contribution of Ca 2+ influx through the activation of I Ca,L to the activation of I K(Ca) A bell-shaped relationship between the conditioning potentials and the integrated I K(Ca) was observed, suggesting that the magnitude of integrated I Ca,L correlates well with that of integrated I K(Ca) in the same cell. A linear relationship of integrated I Ca,L and integrated I K(Ca) was found with a coupling ratio of 69 ± 7. The value of the coupling ratio was unaffected by the presence of Bay K 8644 or nimodipine, although these compounds could effectively affect the amplitudes of both I K(Ca) and I Ca,L. However, tetrandrine could decrease the coupling ratio. Paxilline or intracellular Ca 2+ buffer with EGTA decreased the coupling ratio, while apamin had no effect on it. Interestingly, phorbol 12-myristate 13-acetate also reduced the coupling ratio significantly, whereas thapsigargin increased this value. Thus, the present study indicates that the activation of I K(Ca) during brief Ca 2+ influx, which is inhibited by paxilline, is coupled to Ca 2+ influx primarily through the L-type channels. The selective modulation of I K(Ca) by second messengers or Ca 2+ release from internal stores may affect the coupling efficiency and hence cellular excitability.
|Number of pages||7|
|Journal||Chinese Journal of Physiology|
|Publication status||Published - 2001 Jan 1|
All Science Journal Classification (ASJC) codes
- Physiology (medical)