Membrane stretch augments the cardiac muscarinic K+ channel activity |
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Authors: | A. Pleumsamran D. Kim |
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Affiliation: | (1) Department of Physiology and Biophysics, Finch University of Health Sciences Chicago Medical School, 3333 Green Bay Road, 60064 North Chicago, IL |
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Abstract: | Arachidonic acid has been shown to activate K+-selective, mechanosensitive ion channels in cardiac, neuronal and smooth muscle cells. Since the cardiac G protein (GK)-gated, muscarinic K+ (KACh) channel can also be activated by arachidonic acid, we investigated whether the KACh channel was also sensitive to membrane stretch. In the absence of acetylcholine (ACh), KACh channels were not active, and negative pressure failed to activate these channels. With ACh (10 m) in the pipette, applying negative pressure (0 to –80 mm Hg) to the membrane caused a reversible, pressure-dependent increase in channel activity in cell-attached and inside-out patches (100 m GTP in bath). Membrane stretch did not alter the sensitivity of the KACh channel to GTP. When GK was maximally activated with 100 m GTP S in inside-out patches, the KACh channel activity could be further increased by negative pressure. Trypsin (0.5 mg/ ml) applied to the membrane caused activation of the KACh channel in the absence of ACh and GTP; KACh channel activity was further increased by stretch. These results indicate that the atrial muscarinic K+ channels are modulated by stretch independently of receptor/G protein, probably via a direct effect on the channel protein/ lipid bilayer. |
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Keywords: | Mechanosensitivity Arachidonic acid Muscarinic K channel Pressure G protein |
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