Calcium-Sensitive Chloride Channels in Vascular Smooth Muscle Cells

Academic Article

Abstract

  • Chloride (Cl ) channels were characterized in vascular smooth muscle cells (VSMC) using radioisotope flux and patch-clamp electrophysiological techniques. Transmembrane iodine ( l) efflux from subcultured (Passage 1-5) rat aortic VSMCs was used as an indicator of Cl movements to study the relationship between intracellular calcium concentration ([Ca ] ) and CI channel activity. Angiotensin II (Ang II) (10 M) and adenosine 5'-triphosphate (ATP) (10 M) induced rapid increases (9,7- and 14.9-fold, respectively) in I efflux rates. We found that both Ang II-and ATP-stimulated I efflux and [Ca ] increases were completely abolished after brief incubation (20 μM, 20 min) with the acetoxymethyl ester of 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM), a membrane-permeable Ca chelator. However, when external EGTA was used to blunt agonist-stimulated Ca influx, l efflux was still increased in response to Ang II and ATP. These data suggest that Ca release from intracellular sites is sufficient to activate CI channels in response to Ang II and ATP. Using standard patch-clamp electrophysiological techniques, we found that Ang II, a Ca -mobilizing agonist, stimulated outward Cl currents (g = 75 pS) in cell-attached (C/A) patches of primary and subcultured VSMCs. Collectively, these data suggest that Ang II and other vasoconstrictor agents stimulate Cl channel activity via increases in [Ca ] . Cl channel activation may help to depolarize the VSMC membrane leading to increased Ca influx during agonist stimulation. © 1995, SAGE Publications. All rights reserved. - 125 125 - 2+ - -7 -4 125 125 2+ 2+ 2+ 125 2+ - 2+ - - 2+ - 2+ 1 I cl l
  • Authors

    Digital Object Identifier (doi)

    Author List

  • White CR; Elton TS; Shoemaker RL; Brock TA
  • Start Page

  • 255
  • End Page

  • 262
  • Volume

  • 208
  • Issue

  • 3