title: Effects of sodium nitroprusside in the rat cortical collecting duct are independent of the NO pathway.
abstract: 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 (Pflugers Arch 429:338-344, 1995). We examined the effects of the NO-liberator sodium nitroprusside (SNP) on single channel activity and membrane voltage (Vm) 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 SNP (10 microM) hyperpolarized principal cells from -54 +/- 10 mV to -71 +/- 5 mV (N = 5) and increased the activity of the described K+ channels from 0.05 +/- 0.03 to 0.45 +/- 0.14 (N = 5) in cell-attached and from 0.04 +/- 0.02 to 0.25 +/- 0.05 (N = 4) in excised patch clamp experiments, it had no effect on basal or AVP-dependent transepithelial voltage, Na+ fluxes, or the osmotic water permeability. In addition, neither 50 microM SIN-1, another liberator of NO, nor 1 mM L-NAME, an inhibitor of the NO-synthase, changed Vm significantly. Furthermore, in cGMP-assays SNP failed to increase intracellular cGMP in CCD segments. Thus, 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+ channels in the basolateral membrane of these cells.
authors.affiliation: Westfälische Wilhelms-Universität Münster, Med. Poliklinik, Experimentelle Nephrologie, Germany. hirschi@uni-muenster.de
authors.forename: J R
authors.initials: JR
authors.lastname: Hirsch
authors.forename: R
authors.initials: R
authors.lastname: Cermak
authors.forename: W G
authors.initials: WG
authors.lastname: Forssmann
authors.forename: R
authors.initials: R
authors.lastname: Kleta
authors.forename: M
authors.initials: M
authors.lastname: Kruhøffer
authors.forename: M
authors.initials: M
authors.lastname: Kuhn
authors.forename: J A
authors.initials: JA
authors.lastname: Schafer
authors.forename: D
authors.initials: D
authors.lastname: Sun
authors.forename: E
authors.initials: E
authors.lastname: Schlatter
mesh_terms: D000818:Animals; D001127:Arginine Vasopressin / Q000494:pharmacology; D006152:Cyclic GMP / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D066298:In Vitro Techniques; D007672:Kidney Cortex / Q000187:drug effects* / Q000378:metabolism*; D007685:Kidney Tubules, Collecting / Q000187:drug effects* / Q000378:metabolism*; D008564:Membrane Potentials / Q000187:drug effects; D008981:Molsidomine / Q000031:analogs & derivatives / Q000494:pharmacology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D009599:Nitroprusside / Q000494:pharmacology*; D010477:Perfusion; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
chemical_list: D004791:Enzyme Inhibitors; D015221:Potassium Channels; D001127:Arginine Vasopressin; D009599:Nitroprusside; D009569:Nitric Oxide; C002385:linsidomine; D008981:Molsidomine; D019001:Nitric Oxide Synthase; D006152:Cyclic GMP; D019331:NG-Nitroarginine Methyl Ester