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Whether H\n                    <jats:sub>2<\/jats:sub>\n                    S regulates water metabolism in the kidney and the potential mechanism are still unknown. The present study was conducted to determine the role of H\n                    <jats:sub>2<\/jats:sub>\n                    S in urine concentration. Inhibition of both cystathionine\u2010\u03b3\u2010lyase (CSE) and cystathionine\u2010\u03b2\u2010synthase (CBS), 2 major enzymes for endogenous H\n                    <jats:sub>2<\/jats:sub>\n                    S production, with propargylglycine (PPG) and amino\u2010oxyacetate (AOAA), respectively, caused increased urine output and reduced urine osmolality in mice that was associated with decreased expression of aquaporin (AQP)\u20102 in the renal inner medulla. Mice treated with both PPG and AOAA developed a urine concentration defect in response to dehydration that was accompanied by reduced AQP\u20102 protein expression. Inhibition of CSE alone was associated with a mild decrease in AQP\u20102 protein level in the renal medulla of heterozygous CBS mice. GYY4137, a slow H\n                    <jats:sub>2<\/jats:sub>\n                    S donor, markedly improved urine concentration and prevented the down\u2010regulation of renal AQP\u20102 protein expression in mice with lithium\u2010induced nephrogenic diabetes insipidus (NDI). GYY4137 significantly increased cAMP levels in cell lysates prepared from inner medullary collecting duct (IMCD) suspensions. AQP\u20102 protein expression was also upregulated, but was significantly inhibited by the adenyl cyclase inhibitor MDL12330A or the PKA inhibitor H89, but not the vasopressin 2 receptor (V\n                    <jats:sub>2<\/jats:sub>\n                    R) antagonist tolvaptan. Inhibition of endogenous H\n                    <jats:sub>2<\/jats:sub>\n                    S production impaired urine concentration in mice, whereas an exogenous H\n                    <jats:sub>2<\/jats:sub>\n                    S donor improved urine concentration in lithium\u2010induced NDI by increasing AQP\u20102 expression in the collecting duct principal cells. H\n                    <jats:sub>2<\/jats:sub>\n                    S upregulated AQP\u20102 protein expression, probably\n                    <jats:italic>via<\/jats:italic>\n                    the cAMP\u2010PKA pathway.\u2014Luo, R., Hu, S., Liu, Q., Han, M., Wang, F., Qiu, M., Li, S., Li, X., Yang, T., Fu, X., Wang, W., Li, C. Hydrogen sulfide upregulates renal AQP\u20102 protein expression and promotes urine concentration. FASEB J. 33, 469\u2013483 (2019).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.201800436r","type":"journal-article","created":{"date-parts":[[2018,7,23]],"date-time":"2018-07-23T14:49:31Z","timestamp":1532357371000},"page":"469-483","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":40,"title":["Hydrogen sulfide upregulates renal AQP\u20102 protein expression and promotes urine concentration"],"prefix":"10.1096","volume":"33","author":[{"given":"Renfei","family":"Luo","sequence":"first","affiliation":[{"name":"Institute of Hypertension Zhongshan School of Medicine Sun Yat-sen University  Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shan","family":"Hu","sequence":"additional","affiliation":[{"name":"Institute of Hypertension Zhongshan 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