{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T16:55:34Z","timestamp":1792083334536,"version":"4.4.0"},"reference-count":74,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2019,4,4]],"date-time":"2019-04-04T00:00:00Z","timestamp":1554336000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"name":"JSPS KAKENHI","award":["19H03678"],"award-info":[{"award-number":["19H03678"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,6,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>The recent advances in genetics and molecular biology have resulted in the characterization of key components that critically regulate renal NaCl transport and blood pressure. Pendrin is a Cl\u2212\/HCO3\u2212 exchanger that is highly expressed in thyroid, inner ear, and kidney. In the kidney, it is selectively present at the apical membrane in non-\u03b1 intercalated cells of the connecting tubules and cortical collecting duct. Besides its role in acid\/base homeostasis, accumulating studies using various genetically modified animals have provided compelling evidence that pendrin regulates extracellular fluid volume and electrolyte balance at the downstream of aldosterone signaling. We have shown that angiotensin II and aldosterone cooperatively control pendrin abundance partly through mammalian target of rapamycin signaling and mineralocorticoid receptor dephosphorylation, which is necessary for the kidney to prevent extracellular fluid loss and electrolyte disturbances under physiologic perturbations. In line with the experimental observations, several clinical data indicated that the impaired pendrin function can cause fluid and electrolyte abnormalities in humans. The purpose of this review is to provide an update on the recent progress regarding the role of pendrin in fluid and electrolyte homeostasis, as well as in the pathophysiology of hypertension associated with mineralocorticoid receptor signaling.<\/jats:p>","DOI":"10.1093\/ajh\/hpz054","type":"journal-article","created":{"date-parts":[[2019,4,11]],"date-time":"2019-04-11T15:59:04Z","timestamp":1554998344000},"page":"607-613","source":"Crossref","is-referenced-by-count":7,"title":["Role of Pendrin in the Pathophysiology of Aldosterone-Induced Hypertension"],"prefix":"10.1093","volume":"32","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6868-0626","authenticated-orcid":false,"given":"Shigeru","family":"Shibata","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2019,4,4]]},"reference":[{"key":"2022110919181527700_CIT0001","doi-asserted-by":"crossref","first-page":"135","DOI":"10.2215\/CJN.05760513","article-title":"Collecting duct principal cell transport processes and their regulation","volume":"10","author":"Pearce","year":"2015","journal-title":"Clin J Am Soc Nephrol"},{"key":"2022110919181527700_CIT0002","doi-asserted-by":"crossref","first-page":"363","DOI":"10.1146\/annurev-physiol-021014-071854","article-title":"The role of pendrin in renal physiology","volume":"77","author":"Wall","year":"2015","journal-title":"Annu Rev Physiol"},{"key":"2022110919181527700_CIT0003","doi-asserted-by":"crossref","first-page":"1627","DOI":"10.1152\/physrev.00038.2017","article-title":"Angiotensin II signal transduction: an update on mechanisms of physiology and pathophysiology","volume":"98","author":"Forrester","year":"2018","journal-title":"Physiol Rev"},{"key":"2022110919181527700_CIT0004","doi-asserted-by":"crossref","first-page":"333","DOI":"10.1007\/BF02155834","article-title":"Isolation from the adrenals of a new crystalline hormone with especially high effectiveness on mineral metabolism","volume":"9","author":"Simpson","year":"1953","journal-title":"Experientia"},{"key":"2022110919181527700_CIT0005","first-page":"661","article-title":"Primary aldosteronism","volume":"45","author":"Conn","year":"1955","journal-title":"J Lab Clin Med"},{"key":"2022110919181527700_CIT0006","doi-asserted-by":"crossref","first-page":"234","DOI":"10.1001\/jama.1960.03030030014003","article-title":"Hypotensive agents and pressor substances. 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