ADRENERGIC REGULATION OF CALCIUM-ACTIVATED POTASSIUM CURRENT IN CULTURED RABBIT PIGMENTED CILIARY EPITHELIAL-CELLS

1. The effects of adrenergic agonists on K+ currents were studied in c ultured rabbit pigmented ciliary epithelial (PCE) cells. 2. Outward K current (I-K) was reduced by tetraethylammonium chloride, the Ca2+-ac tivated K+ (K(Ca)) channel blocker iberiotoxin (IbTX), or Ca2+-free ex ternal Ringer solution. The calcium ionophore ionomycin increased an I bTX-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 alpha(1)-antagonist prazosin, suggesting that adrenergic agonists activate I-K(Ca) via alpha(1)-adrenoreceptors. 4. Internal dialysis of D-myo-inositol 1,4,5-trisphosphate (IP3) increase d I-K, whilst pre incubation of PCE cells with thapsigargin or the pho spholipase C (PLC) inhibitor U-73122 reduced phenylephrine-induced inc reases in I-K(Ca). Adrenergic increases in I-K(Ca) were mediated by a pertussis toxin-insensitive G protein. 5. These results demonstrate th at I-K(Ca) channels in rabbit PCE cells are coupled to alpha(1)-adrene rgic receptors and a PLC/IP3 signalling pathway. Activation of these c hannels may modulate fluid secretion by the ciliary epithelium.