ArticleFrontiers in pharmacology2026
Loss of OXGR1 function uncouples intrarenal RAS activation from pendrin and αENaC regulation and blunts angiotensin II-induced hypertension.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Activation of the intrarenal renin-angiotensin system (RAS) is a key mechanism driving sodium retention and hypertension. In the distal nephron, locally generated angiotensin II (Ang II) promotes Na Methods: mice were subjected to chronic Ang II infusion (400 ng·min Results: Ang II infusion increased blood pressure, promoted antinatriuresis, and elevated intrarenal Ang II, ACE activity, PRR, pendrin, and αENaC protein abundance. In contrast, both montelukast-treated wild type and OXGR1 Conclusion: These findings identify OXGR1 as a critical regulator linking intrarenal RAS activation to distal nephron Na
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