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Adrenergic regulation of calcium‐activated potassium current in cultured rabbit pigmented ciliary epithelial cells
Author(s) -
Ryan Jennifer S.,
Tao QianPing,
Kelly Melanie E. M.
Publication year - 1998
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1998.145bi.x
Subject(s) - rabbit (cipher) , calcium , potassium , chemistry , microbiology and biotechnology , ciliary processes , adrenergic , endocrinology , ciliary body , medicine , biophysics , biology , biochemistry , neuroscience , receptor , statistics , mathematics , organic chemistry
1 The effects of adrenergic agonists on K + currents were studied in cultured rabbit pigmented ciliary epithelial (PCE) cells. 2 Outward K + current ( I K ) was reduced by tetraethylammonium chloride, the Ca 2+ ‐activated K + (K(Ca)) channel blocker iberiotoxin (IbTX), or Ca 2+ ‐free external Ringer solution. The calcium ionophore ionomycin increased an IbTX‐sensitive I K in PCE cells. 3 The adrenergic agonists adrenaline and phenylephrine increased I K in PCE cells. The induced current was blocked by IbTX and the α 1 ‐antagonist prazosin, suggesting that adrenergic agonists activate I K(Ca) via α 1 ‐adrenoreceptors. 4 Internal dialysis of D‐ myo ‐inositol 1,4,5‐trisphosphate (IP 3 ) increased I K , whilst pre‐incubation of PCE cells with thapsigargin or the phospholipase C (PLC) inhibitor U‐73122 reduced phenylephrine‐induced increases in I K(Ca) . Adrenergic increases in I K(Ca) were mediated by a pertussis toxin‐insensitive G protein. 5 These results demonstrate that I K(Ca) channels in rabbit PCE cells are coupled to α 1 ‐adrenergic receptors and a PLC/IP 3 signalling pathway. Activation of these channels may modulate fluid secretion by the ciliary epithelium.