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Exploring Arterial Smooth Muscle Kv7 Potassium Channel Function using Patch Clamp Electrophysiology and Pressure Myography
Published on: September 14, 2012
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Membrane depolarization activates BK channels through ROCK-mediated β1 subunit surface trafficking to limit
M Dennis Leo1, Xue Zhai1, Padmapriya Muralidharan1
1Department of Physiology, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Science Signaling
|May 11, 2017
Summary
Membrane depolarization triggers vasoconstriction but also activates large-conductance calcium-activated potassium (BK) channels. This study reveals how BK channel activity is enhanced, promoting vasodilation in arterial myocytes.
Area of Science:
- Cardiovascular Physiology
- Molecular Cell Biology
- Smooth Muscle Physiology
Background:
- Membrane depolarization of arterial smooth muscle cells causes vasoconstriction.
- Large-conductance calcium-activated potassium (BK) channels regulate this process, promoting vasodilation by counteracting calcium channel activity.
Purpose of the Study:
- To elucidate the mechanism by which membrane depolarization enhances BK channel activity in arterial myocytes.
- To investigate the role of BK channel auxiliary subunits and their trafficking in regulating vascular tone.
Main Methods:
- Studied human and rat arterial myocytes.
- Assessed changes in cell surface BK channel subunit abundance following membrane depolarization.
- Investigated the involvement of calcium influx, Rho kinase (ROCK) signaling, and Rab11A-mediated trafficking.
Main Results:
- Membrane depolarization increased the cell surface abundance of BK β1 subunits, not BKα channels.
- Calcium influx activated ROCK1/2, which in turn activated Rab11A.
- Rab11A mediated the delivery of β1 subunits to the plasma membrane, increasing BK channel activity and causing vasodilation.
Conclusions:
- Membrane depolarization activates BK channels via ROCK- and Rab11A-dependent trafficking of β1 subunits to the myocyte surface.
- This mechanism enhances BK channel activity, contributing to vasodilation in small arteries.
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