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We used patch-clamp techniques to examine whether nitric oxide (NO) decreases NaCl reabsorption by suppressing basolateral 10-pS Cl −  channels in the thick ascending limb (TAL). Both the NO synthase substrate l-arginine (l-Arg) and the NO donor S-nitroso- N-acetylpenicillamine significantly inhibited 10-pS Cl −  channel activity in the TAL. The inhibitory effect of l-Arg on Cl −  channels was completely abolished in the presence of the NO synthase inhibitor or NO scavenger. Moreover, inhibition of soluble guanylyl cyclase abrogated the effect of l-Arg on Cl −  channels, whereas the cGMP analog 8-bromo-cGMP (8-BrcGMP) mimicked the effect of l-Arg and significantly decreased 10-pS Cl −  channel activity, indicating that NO inhibits basolateral Cl −  channels by increasing cGMP production. Furthermore, treatment of the TAL with a PKG inhibitor blocked the effect of l-Arg and 8-BrcGMP on Cl −  channels, respectively. In contrast, a phosphodiesterase 2 inhibitor had no significant effect on l-Arg or 8-BrcGMP-induced inhibition of Cl −  channels. Therefore, we conclude that NO decreases basolateral 10-pS Cl −  channel activity through a cGMP-dependent PKG pathway, which may contribute to the natriuretic and diuretic effects of NO in vivo.

Nitric oxide inhibits basolateral 10-pS Cl−channels through the cGMP/PKG signaling pathway in the thick ascending limb of C57BL/6 mice

Nitric oxide inhibits basolateral 10-pS Cl⁻channels through the cGMP/PKG signaling pathway in the thick ascending limb of C57BL/6 mice