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

American Journal of Physiology. Renal Physiology
Peng WuZhi Qi

Abstract

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.

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Citations

Mar 10, 2017·American Journal of Physiology. Renal Physiology·Casandra M MonzonJeffrey L Garvin
Oct 26, 2018·Physiological Reviews·Agustin Gonzalez-VicenteJeffrey L Garvin

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