Cardiovascular System

Pflügers Archiv

, Volume 446, Issue 5, pp 523-528

First online:

Actin filaments regulate the stretch sensitivity of large-conductance, Ca2+-activated K+ channels in coronary artery smooth muscle cells

  • Lin PiaoAffiliated withNational Research Laboratory for Cellular Signalling and Department of Physiology, Seoul National University College of Medicine
  • , Won-Kyung HoAffiliated withNational Research Laboratory for Cellular Signalling and Department of Physiology, Seoul National University College of Medicine
  • , Yung E. EarmAffiliated withNational Research Laboratory for Cellular Signalling and Department of Physiology, Seoul National University College of Medicine Email author 

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Abstract

Using the inside-out patch-clamp technique, large-conductance Ca2+-activated K+ channel (BKCa) currents were recorded from coronary artery smooth muscle cells. Cytochalasin D, an actin filament disrupter, increased channel activity (NP o, where N is the number of channels and P o the open probability), and this increase was reversed by phalloidin, an actin filament stabilizer. NP o was also increased by colchicine, a microtubule disrupter, and decreased by taxol, a microtubule stabilizer. With the stepwise increase of negative pressure in the patch pipettes, the activity of BKCa gradually increased: the maximum effect (527% increase in NP o) was achieved at −40 cmH2O and the half-maximum effect at −25 cmH2O. The increase in NP o in response to negative pressure was abolished by phalloidin but not by taxol. These results imply that both actin filaments and microtubules inhibit the opening of BKCa in coronary artery smooth muscle cells, but that only actin filaments are involved in the stretch sensitivity of BKCa.

Keywords

Vascular smooth muscle Ca2+-activated K+ channel Membrane stretch Cytoskeleton Actin filaments Microtubules