AIM: To investigate the effect of actin microfilament on potassium current and hyposmotic membrane stretch-induced increase of potassium current in gastric antral circular myocytes of guinea pig. METHODS: Whole-cell patch clamp technique was used to record potassium current in isolated gastric myocyes. RESULTS: When the membrane potential was clamped at -60 mV, an actin microfilament disruptor, cytochanlasin-B(Cyt-B, 20 micromol/L in pipette) increased calcium-activated potassium current (I(K(Ca))) and delayed rectifier potassium current (I(K(V))) to 138.4+/-14.3% and 142.1+/-13.1% respectively at +60 mV. In the same condition, an actin microfilament stabilizer phalloidin (20 micromol/L in pipette) inhibited I(K(Ca)) and I(K(V)) to 74.2+/-7.1% and 75.4+/-9.9% respectively. At the holding potential of -60 mV, hyposmotic membrane stretch increased I(K(Ca)) and I(K(V)) by 50.6+/-9.7% and 24.9+/-3.3% at +60 mV respectively. In the presence of cytochalasin-B and phalloidin (20 micromol/L, in the pipette) condition, hyposmotic membrane stretch also increased I(K(Ca)) by 44.5+/-7.9% and 55.7+/-9.8% at +60 mV respectively. In the same condition, cytochalasin-B and phalloidin also increased I(K(V)) by 23.0+/-5.5% and 30.3+/-4.5% respectively. However, Cyt-B and phalloidin did not affect the amplitude of hyposmotic membrane stretch-induced increase of I(K(Ca)) and I(K(V)). CONCLUSION: Actin microfilaments regulate the activities of potassium channels, but they are not involved in the process of hyposmotic membrane stretch-induced increase of potassium currents in gastric antral circular myocytes of guinea pig.
AIM: To investigate the effect of actin microfilament on potassium current and hyposmotic membrane stretch-induced increase of potassium current in gastric antral circular myocytes of guinea pig. METHODS: Whole-cell patch clamp technique was used to record potassium current in isolated gastric myocyes. RESULTS: When the membrane potential was clamped at -60 mV, an actin microfilament disruptor, cytochanlasin-B(Cyt-B, 20 micromol/L in pipette) increased calcium-activated potassium current (I(K(Ca))) and delayed rectifier potassium current (I(K(V))) to 138.4+/-14.3% and 142.1+/-13.1% respectively at +60 mV. In the same condition, an actin microfilament stabilizer phalloidin (20 micromol/L in pipette) inhibited I(K(Ca)) and I(K(V)) to 74.2+/-7.1% and 75.4+/-9.9% respectively. At the holding potential of -60 mV, hyposmotic membrane stretch increased I(K(Ca)) and I(K(V)) by 50.6+/-9.7% and 24.9+/-3.3% at +60 mV respectively. In the presence of cytochalasin-B and phalloidin (20 micromol/L, in the pipette) condition, hyposmotic membrane stretch also increased I(K(Ca)) by 44.5+/-7.9% and 55.7+/-9.8% at +60 mV respectively. In the same condition, cytochalasin-B and phalloidin also increased I(K(V)) by 23.0+/-5.5% and 30.3+/-4.5% respectively. However, Cyt-B and phalloidin did not affect the amplitude of hyposmotic membrane stretch-induced increase of I(K(Ca)) and I(K(V)). CONCLUSION: Actin microfilaments regulate the activities of potassium channels, but they are not involved in the process of hyposmotic membrane stretch-induced increase of potassium currents in gastric antral circular myocytes of guinea pig.