The control of chloride conductance in rat parotid isolated acinar cells investigated by photorelease of caged compounds.

The control of Cl- conductance in rat parotid isolated acinar cells was studied by combined use of whole-cell recording and flash photolysis techniques. Cells were voltage-clamped either at a membrane potential of -40 mV or stepped between -85 mV and 0 mV. Bath-applied carbachol and noradrenaline evoked Cl- current at -85 mV and K+ current at 0 mV. Similar current activations resulted from the photolytic release of either inositol trisphosphate (InsP3) or Ca2+ by a brief near-UV flash. The peak amplitudes of the Cl- conductance (at -85 mV), measured relative to the K+ conductance (at 0 mV), evoked by application of carbachol, noradrenaline or direct manipulation of cytosolic free calcium ([Ca2+]i), were very similar, being 0.56 +/- 0.09 (mean +/- SEM, n = 9), 0.52 +/- 0.01 (n = 7) and 0.46 +/- 0.06 (n = 7). In contrast, the relative amplitude of the Cl- conductance evoked by InsP3 was much larger: 1.49 +/- 0.24 (n = 9). Neither bath application of isoprenaline nor photolysis of "caged" cAMP induced any detectable membrane current. The most probable interpretation of these results is that the observed activation of Cl- conductance by agonists can be explained by the elevation of [Ca2+]i alone. In addition, the present results provide further support for the previously reported suggestion that the Cl- channels and the Ca(2+)-release sites are co-localised [10].