The effect of the nitric oxide (NO) pathway on K⁺ (measured using ⁸⁶Rb) transport in adult rat distal colon was investigated in muscle-stripped segments of colons mounted in Ussing chambers. When added to the mucosal solution, the endogenous precursor of NO, L-arginine (30 mM), inhibited both mucosal-to-serosal and serosal-to-mucosal ⁸⁶Rb fluxes and caused a prolonged decrease of short-circuit current (I_sc). This effect was significantly reduced by the NO synthase inhibitor N^G-nitro-L-arginine methyl ester (L-NAME) but not by D-NAME. Mucosal application of S-nitroso-N-acetyl-penicillamine (SNAP) inhibited mucosal-to-serosal ⁸⁶Rb flux without affecting serosal-to-mucosal transport. Serosal addition of two different exogenous NO donors, sodium nitroprusside (0.1 mM) and SNAP (0.2 mM), decreased serosal-to-mucosal ⁸⁶Rb flux, whereas I_sc increased. The SNAP-induced decrease in ⁸⁶Rb flux was abolished by 1H-(1,2,4)oxodiazolo(4,3-a)quinoxalin-1-one (0.2 mM), a selective inhibitor of NO-stimulated soluble guanylyl cyclase, and by methylene blue (0.01 mM). Addition of 8-bromo-cGMP (2 × 10⁴ M) in the presence of an inhibitor of cGMP-specific phosphodiesterase mimicked the effects of NO-donating compounds. This study provides evidence that NO inhibits K⁺ transport in the rat distal colon via a cGMP-dependent pathway. The effect on net K⁺ transport may depend on the side of NO action.

nitric oxide donors; guanosine 3',5'-cyclic monophosphate pathway

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