CGMP-ACTIVATING PEPTIDES DO NOT REGULATE ELECTROGENIC ELECTROLYTE TRANSPORT IN PRINCIPAL CELLS OF RAT CCD

K+ channels in the basolateral membrane of rat cortical collecting duc t (CCD) are regulated by a cGMP-dependent protein kinase (J. Hirsch an d E. Schlatter. Pfluegers Arch. 429: 338-344, 1995). Conflicting data exist on the effects of cGMP-activating agonists on Na+ transport in t hese cells. Thus we tested members of the family of peptides that incr ease intracellular cGMP [cardiodilatin/atrial natriuretic peptide (CDD /ANP), brain natriuretic peptide, C-type natriuretic peptide, urodilat in, guanylin, and uroguanylin], as well as bradykinin +/- CDD/ANP on m embrane voltages (V-m) of principal cells of isolated rat CCD using th e slow whole cell patch-clamp technique (E. Schlatter, V. Frobe, and R . Greger. Pfluegers Arch. 421: 381-387, 1992). None of the agonists te sted changed V-m significantly. There was also no effect of dibutyryl guanosine 3',5'-cyclic monophosphate (DBcGMP) on AVP-dependent lumen-t o-bath Na+ flux, transepithelial voltage, or osmotic water permeabilit y in isolated perfused rat CCD. Finally, CDD/ANP increased intracellul ar cGMP only in glomeruli but not in CCD. Thus the findings provide no evidence for control of electrogenic electrolyte transport by these n atriuretic peptides in principal cells of rat CCD, and the agonist tha t physiologically regulates the cGMP-dependent K+ channels remains to be identified.