Published online Nov 15, 2004. doi: 10.3748/wjg.v10.i22.3303
Revised: March 4, 2004
Accepted: March 18, 2004
Published online: November 15, 2004
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 μmol/L in pipette) increased calcium-activated potassium current (IK(Ca)) and delayed rectifier potassium current (IK(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 μmol/L in pipette) inhibited IK(Ca) and IK(V) to 74.2% ± 7.1% and 75.4% ± 9.9% respectively. At the holding potential of -60 mV, hyposmotic membrane stretch increased IK(Ca) and IK(V) by 50.6% ± 9.7% and 24.9% ± 3.3% at +60 mV respectively. In the presence of cytochalasin-B and phalloidin (20 μmol/L, in the pipette) condition, hyposmotic membrane stretch also increased IK(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 IK(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 IK(Ca) and IK(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.