EFFECTS OF SODIUM-NITROPRUSSIDE IN THE RAT CORTICAL COLLECTING DUCT ARE INDEPENDENT OF THE NO PATHWAY

Effects of sodium nitroprusside in the rat cortical collecting duct ar e independent of the NO pathway, Recently we described K+ channels in the basolateral membrane of principal cells of rat cortical collecting duct (CCD) which are regulated by a cGMP-dependent protein kinase (Pf lugers Arch 429:338-344, 1995). We examined the effects of the NO-libe rator sodium nitroprusside (SNP) on single channel activity and membra ne voltage (V-m) in principal cells of rat CCD, and on transepithelial voltage, lumen-to-bath Na+ fluxes, and osmotic water permeability in isolated perfused rat CCD tubules. While in patch clamp experiments SN P (10 mu M) hyperpolarized principal cells from -54 +/- 10 mV to -71 /- 5 mV (N = 5) and increased the activity of the described K+ channel s from 0.05 +/- 0.03 to 0.45 +/- 0.14 (N = 5) in cell-attached and fro m 0.04 +/- 0.02 to 0.25 +/- 0.05 (N = 4) in excised patch clamp experi ments, it had no effect on basal or AVP-dependent transepithelial volt age, Na+ fluxes, or the osmotic water permeability. In addition, neith er 50 mu M SIN-1, another liberator of NO, nor 1 mM L-NAME, an inhibit or of the NO-synthase, changed V-m significantly. Furthermore, in cGMP -assays SNP failed to increase intracellular cGMP in CCD segments. Thu s, we conclude that in the rat CCD transport is not regulated via the NO-pathway and that SNP acts as an cGMP independent activator of K+ ch annels in the basolateral membrane of these cells.