AIM： Interstitial cells of Cajal （ICCs） are the pacemaker cells that generate slow waves in the gastrointestinal （GI） tract. We have aimed to investigate the involvement of mitochondrial Na^＋-Ca^2＋ exchange in ...AIM： Interstitial cells of Cajal （ICCs） are the pacemaker cells that generate slow waves in the gastrointestinal （GI） tract. We have aimed to investigate the involvement of mitochondrial Na^＋-Ca^2＋ exchange in intestinal pacemaking activity in cultured interstitial cells of Cajal. METHODS： Enzymatic digestions were used to dissociate ICCs from the small intestine of a mouse. The whole-cell patch-clamp configuration was used to record membrane currents （voltage clamp） and potentials （current clamp） from cultured ICCs. RESULTS： Clonazepam and CGP37157 inhibited the pacemaking activity of ICCs in a dose-dependent manner. Clonazepam from 20 to 60 μmol/L and CGP37157 from 10 to 30 μmol/L effectively inhibited Ca^2＋ efflux from mitochondria in pacemaking activity of ICCs. The ICsos of clonazepam and CGP37157 were 37.1 and 18.2 μmol/ L, respectively. The addition of 20 μmol/L NiCl2 to the internal solution caused a ＂wax and wane＂ phenomenon of pacemaking activity of ICCs. CONCLUSION： These results suggest that mitochondria Na^＋-Ca^2＋ exchange has an important role in intestina pacemaking activity.展开更多
Results from a systematic experiment on isolated perfused rat heart and isolated myc-cytes of adult rat showed that the mechanism of calcium influx during myocardial ischemia-reperfusion is due to the development of i...Results from a systematic experiment on isolated perfused rat heart and isolated myc-cytes of adult rat showed that the mechanism of calcium influx during myocardial ischemia-reperfusion is due to the development of intracellular sodium overload during ischemic pe-riod, on reperfusion, the high intracellular Na^+ content activated the reverse direction ofNa^+-Ca^(2+) exchange over myocardial sarcolemma (SL), thus a large quantity of extracellularCa^(2+) fluxed over the SL to the intracellular space, forming a condition of intracellular Ca^(2+)overload, which leads to irreversible damage of the myocardium.展开更多
基金Supported by the Seoul National University Hospital Research Fund(03-2004-008)Korea Research Foundation Grant funded by Korea Government(MOEHRD,Basic Research Promotion Fund,KRF-2004-041-E00022)BK21 project for medicine,dentistry,and pharmacy
文摘AIM： Interstitial cells of Cajal （ICCs） are the pacemaker cells that generate slow waves in the gastrointestinal （GI） tract. We have aimed to investigate the involvement of mitochondrial Na^＋-Ca^2＋ exchange in intestinal pacemaking activity in cultured interstitial cells of Cajal. METHODS： Enzymatic digestions were used to dissociate ICCs from the small intestine of a mouse. The whole-cell patch-clamp configuration was used to record membrane currents （voltage clamp） and potentials （current clamp） from cultured ICCs. RESULTS： Clonazepam and CGP37157 inhibited the pacemaking activity of ICCs in a dose-dependent manner. Clonazepam from 20 to 60 μmol/L and CGP37157 from 10 to 30 μmol/L effectively inhibited Ca^2＋ efflux from mitochondria in pacemaking activity of ICCs. The ICsos of clonazepam and CGP37157 were 37.1 and 18.2 μmol/ L, respectively. The addition of 20 μmol/L NiCl2 to the internal solution caused a ＂wax and wane＂ phenomenon of pacemaking activity of ICCs. CONCLUSION： These results suggest that mitochondria Na^＋-Ca^2＋ exchange has an important role in intestina pacemaking activity.
基金"7-5 project" supported by the National Research Foundation of China.
文摘Results from a systematic experiment on isolated perfused rat heart and isolated myc-cytes of adult rat showed that the mechanism of calcium influx during myocardial ischemia-reperfusion is due to the development of intracellular sodium overload during ischemic pe-riod, on reperfusion, the high intracellular Na^+ content activated the reverse direction ofNa^+-Ca^(2+) exchange over myocardial sarcolemma (SL), thus a large quantity of extracellularCa^(2+) fluxed over the SL to the intracellular space, forming a condition of intracellular Ca^(2+)overload, which leads to irreversible damage of the myocardium.
