Abstract
The aim of this study is to elucidate the functional role of large conductance, stretch-activated, Ca2+-activated K+ (SAKca) channel originally cloned from cultured chick ventricular myocytes (CCVM). We previously demonstrated that SAKca channel can be activated by membrane stretch as well as membrane depolarization and intracellular calcium. However, the physiological importance of SAKca channel in cardiovascular system remains unknown. To pursue the functional role of cardiac SAKca channel, conventional whole-cell patch-clamp techniques were applied to human embryonic kidney (HEK293) cell lines transfecting cloned SAKca genes and CCVM (isolated from chick embryos 10 day old). These recordings show that the voltage dependent outward currents in CCVM as well as the HEK 293 cell lines were inhibited by BK channel specific blocker charybdotoxin (ChTX, 10 nM). Thus, we hypothesized that ChTX could prolong the repolarization phase of action potentials (APs) of CCVM. To clarify this hypothesis, we recorded evoked APs of CCVM in the whole-cell current clamp technique, and examined the effects of ChTX on the APs. The results show that repolarization phases of evoked APs were not affected by ChTX (30 nM). The series of results implied that SAKca channels in CCVM could not at least activated in physiological conditions but possibly in pathophysiological conditions such as overloading of mechanical stimuli and/or hypoxia, and might play some defensive roles against prolongation of repolarization phase on APs in these conditions. [J Physiol Sci. 2007;57 Suppl:S222]
