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Endothelin increases single‐channel calcium currents in coronary arterial smooth muscle cells
Author(s) -
Silberberg Shai D.,
Poder Thomas C.,
Lacerda Antonio E.
Publication year - 1989
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(89)81242-6
Subject(s) - calcium , extracellular , biophysics , chemistry , patch clamp , endothelin receptor , vascular smooth muscle , t type calcium channel , calcium channel , voltage dependent calcium channel , endothelin 1 , ion channel , medicine , membrane potential , endocrinology , smooth muscle , biology , biochemistry , receptor
Endothelin (ET), a newly identified vasoconstrictor peptide produced by endothelial cells, depends on extracellular calcium for its action [(1988) Nature 332, 411–415]. It is not yet known whether the increase in calcium influx induced by ET results from a direct effect on the Ca 2+ channels or is secondary to a reduction in membrane potential. To address this question, we studied the effects of ET on single‐channel calcium currents of freshly dissociated porcine coronary artery smooth muscle cells using the cell‐attached mode of the patch‐clamp technique. We show that ET increases Cal + ‐channel activity with no effect on channel open time or conductance. The ability of bath‐applied ET to increase single‐channel calcium currents in the cell‐attached mode is evidence that the peptide acts via a second messenger system.