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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Thiazide diuretics, which inhibit the sodium chloride cotransporter (NCC) in the distal convoluted tubules, are widely used for the treatment of hypertension and heart failure. However, treatment resistance is sometimes observed during long-term thiazide therapy, often accompanied by RAAS activation and hypokalemic alkalosis. Recent studies in artificial animal models of RAAS activation have shown that NCC inhibition or depletion leads to exacerbated activation of RAAS and hypokalemic alkalosis, causing further activation of sodium chloride reabsorption mechanisms in other distal nephron segments, such as the epithelial sodium channel (ENaC) in principal cells and pendrin in beta-intercalated cells. This responce is presumed to contribute to treatment resistance. Here, we analyzed the distal nephron response following thiazide diuretic administration in a mouse model of pressure overload-induced heart failure as a more physiologically relevant disease model.
Male C57BL/6J mice underwent either minimally invasive transverse aortic constriction (TAC) or sham surgery at 13 weeks of age. Two weeks after surgery, all mice were fed a high-salt diet. TAC mice were then assigned to receive either vehicle or hydrochlorothiazide (HCTZ) in their drinking water for 5 weeks.
7 weeks after surgery, TAC induced cardiac hypertrophy in high-salt fed mice, which was attenuated by HCTZ treatment. Renal gene expression of renin and alpha-ENaC tended to be increased by TAC, and this increase was significantly more prominent in the HCTZ-treated group, suggesting RAAS activation. Consistent with RAAS activation, gene expression of pendrin was also significantly increased by HCTZ treatment. Furthermore, changes in the expression of genes associated with the activation of α-ketoglutarate-OXGR1 pathway, which is implicated in alkalosis-dependent pendrin expression, were observed in the HCTZ-treated group.
In heart failure, thiazide therapy may induce counter-activation of distal nephron sodium chloride reabsorption mechanisms via RAAS activation and pathways associated with alkalosis, which potentially lead to treatment resistance.
