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 cultured rabbit pigmented ciliary epithelial (PCE) cells. 2. Outward K⁺ current (I(K)) was reduced by tetraethylammonium chloride, the Ca²⁺-activated K⁺ (K(Ca)) channel blocker iberiotoxin (IbTX), or Ca²⁺-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 α₁-antagonist prazosin, suggesting that adrenergic agonists activate I(K(Ca)) via α₁-adrenoreceptors. 4. Internal dialysis of D-myo-inositol 1,4,5-trisphosphate (IP₃) 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 α₁-adrenergic receptors and a PLC/IP₃ signalling pathway. Activation of these channels may modulate fluid secretion by the ciliary epithelium.