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Mechanical effects on KATP channel gating in rat ventricular myocytes
Haixia Huang1, Lifang Liang, Ping Liu
1Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Plos One
|May 22, 2013
Summary
Cardiac KATP channels, crucial for heart function, are modulated by the actin cytoskeleton. Disrupting actin increases channel activity, suggesting a role in mechanical regulation of heart electrical activity.
Area of Science:
- Cardiovascular Physiology
- Molecular Cardiology
- Cellular Biophysics
Background:
- Cardiac ATP-sensitive potassium (KATP) channels are key regulators linking cellular metabolism to electrical activity in the heart.
- These channels play critical roles in cardiac protection against hypertrophy and failure, and in the secretion of atrial natriuretic peptide.
- Emerging evidence suggests that KATP channels are mechanosensitive, responding to mechanical stimuli, which may be relevant to their physiological functions.
Purpose of the Study:
- To investigate the role of the cortical actin cytoskeleton in modulating the activity and mechanosensitivity of cardiac KATP channels.
- To determine if local membrane tension, influenced by F-actin, affects KATP channel function in rat ventricular myocytes.
Main Methods:
- Utilized inside-out patch-clamp electrophysiology on rat ventricular myocytes to measure KATP channel background activity and stretch sensitivity.
- Compared channel activity and response to mechanical stretch before and after disrupting the cortical F-actin cytoskeleton.
Main Results:
- Disruption of the cortical F-actin significantly potentiated the background activity of cardiac KATP channels.
- Mechanical stretch sensitivity, assessed by the slope of the NPo vs. suction relationship, was not significantly altered by F-actin disruption.
- These findings suggest that actin influences the baseline (prestress) on the channel rather than its dynamic response to stretch.
Conclusions:
- The cortical actin cytoskeleton plays a significant role in regulating the basal activity of cardiac KATP channels.
- Actin likely modulates KATP channel function through parallel elastic sharing of cortical tension with the lipid bilayer, affecting prestress.
- This mechanism highlights a novel pathway for mechanical modulation of cardiac electrical activity via the interplay between actin and KATP channels.
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