Sands J M, Nonoguchi H, Knepper M A
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892.
Am J Physiol. 1988 Sep;255(3 Pt 2):F421-8. doi: 10.1152/ajprenal.1988.255.3.F421.
It has been proposed that regulation of NaCl excretion occurs in part by hormonal effects on NaCl permeability in the inner medullary collecting duct (IMCD). We carried out experiments in isolated perfused terminal IMCDs to determine whether atrial natriuretic factor (ANF), vasopressin, or deoxycorticosterone (DOC) affects NaCl permeability. Apparent Cl- or Na+ permeabilities (PCl and PNa) were determined by measuring ion fluxes resulting from imposed electrochemical gradients. Transepithelial resistance (RT) was calculated from voltage deflections at the perfusion and collection ends of the tubule, which resulted from perfusion end current injection (cable analysis). ANF [rat ANF-(1-28), 100 nM in the peritubular bath] significantly decreased PCl from 2.20 to 1.84 x 10(-5) cm/s and did not alter PNa (1.11 to 1.18 x 10(-5) cm/s). ANF also decreased PCl in IMCDs from DOC-treated rats (1.14 to 0.98 x 10(-5) cm/s). Vasopressin (10 nM in the peritubular bath) did not affect PCl. RT averaged 39.3 omega.cm2 in IMCDs from control rats and was significantly increased to 62.3 omega.cm2 in tubules from DOC-treated rats. Neither ANF nor vasopressin significantly affected RT in either group. We conclude the following: 1) the results do not support the hypothesis that ANF causes natriuresis by increasing the NaCl permeability of the terminal IMCD. Instead, ANF significantly decreases the chloride permeability. 2) Vasopressin does not affect NaCl permeability. 3) Mineralocorticoid-induced antinatriuresis may be due in part to reduced NaCl permeability in the terminal IMCD.
