Pendrin is upregulated by corticosterone and participates in its pressor response.

ABSTRACT: NaCl restriction upregulates pendrin, in part, through increased circulating aldosterone and the intercalated cell (IC) mineralocorticoid receptor (MR). Since 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) enhances aldosterone binding to this receptor in other cells, we asked if pendrin abundance is reduced in NaCl-restricted 11β-HSD2 knockout (KO) rats. However, pendrin abundance was greater in 11β-HSD2 KOs than in controls, possibly from enhanced glucocorticoid MR activation. Moreover, the MR antagonist, spironolactone, reduced pendrin abundance in mice that do not produce aldosterone (aldosterone synthase KO). IC MR gene ablation also reduced pendrin protein abundance in corticosterone-treated, adrenalectomized mice. Therefore, the MR regulates pendrin independently of aldosterone.

SUBMITTER: Pham TD 

PROVIDER: S-EPMC12867009 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature