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. 2017 Aug 30;7:9938. doi: 10.1038/s41598-017-09275-1

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Correlation of intradisulfide formation in endogenous PKGIα with HNO-mediated vasorelaxation in vivo. Both HNO donors induced concentration-dependent dilations in arterioles in vivo. (A) The effect of NCA was studied in 68 vessels from 6 mice. (B) The effect of AS was studied in 73 vessels from 6 mice. Data are given as mean ± SEM. *** indicates P < 0.001 for paired comparisons (t-test). Western immunoblot analysis for PKGIα was performed under reducing (R) and non-reducing (NR) conditions in isolated cremaster muscles exposed to 50 µmol/L NCA or AS. Black arrows indicate the positions of monomeric (75 kDa), inter- (150 kDa) and intradisulfide (below 150 kDa) PKGIα.