Mechanical Effects on K(ATP) Channel Gating in Rat Ventricular Myocytes

Cardiac K(ATP) channels link metabolism with electrical activity. They are implicated in arrhythmias, secretion of atrial natriuretic peptide and protection of the heart from hypertrophy and failure. These processes may involve mechanosensitivity. K(ATP) channels can be activated by mechanical stimulation and disrupting the cortical actin increases the activity. We propose that K(ATP) channels are modulated by local bilayer tension and this tension is affected by cortical F-actin. Here we measured K(ATP) background activity and stretch sensitivity with inside-out patches of rat ventricular myocytes before and after disrupting F-actin. Disrupting F-actin potentiated background activity but did not influence the slope sensitivity in the semilog relationship of NP(o) vs. suction that is a measure of the change in dimensions between closed and open states. Thus actin alters prestress on the channel probably by parallel elastic sharing of mean cortical tension with the bilayer.