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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.
The renal tubular renin-angiotensin system (RAS), via angiotensin II type1 receptor (AT1R) signaling, promote sodium reabsorption, hypertension, and target-organ damage. Sodium transporters such as NCC and ENaC are regulated downstream of this pathway. However, the detailed molecular mechanisms controlling their expression and activity remain incompletely understood. ATRAP (AT1R-associated protein) is an endogenous modulator that suppresses pathological AT1R signaling. We have previously demonstrated that dysregulation of renal ATRAP induces hypertension under various pathological conditions, probably through modulation of sodium transporters (Hypertension 2013; Kidney Int 2014, 2017, 2022; J Biol Chem 2023). In contrast, we have also shown that ATRAP expressed in proximal tubules does not affect blood pressure (J Am Heart Assoc 2019). Based on these findings, we hypothesized that ATRAP in the distal tubules suppress angiotensin II–induced hypertension by inhibiting sodium transporters.
ATRAP cDNA was placed under the control of the Ksp-cadherin promoter and microinjected into C57BL/6 zygotes to generate distal-tubule–specific ATRAP transgenic mice (DT-ATRAP TGM).Overexpression of ATRAP protein was confirmed by Western blotting, and its segment-specific localization was verified by immunostaining using nephron markers such as megalin, calbindin, and AQP2. Blood pressure responses to chronic angiotensin II infusion were compared between DT-ATRAP TGM and wild-type littermates. A diuretic test was also performed to evaluate sodium transporter activity under angiotensin II stimulation. To further elucidate the molecular mechanisms underlying sodium transporter regulation, mouse distal convoluted tubule (mDCT) cells were stably transfected with AT1R and a Tet -inducible ATRAP expression construct. Cells were stimulated with angiotensin II, and transcriptional changes were analyzed by mRNA sequencing.
Among six founder lines, the selected DT-ATRAP TGM line exhibited >10-fold renal ATRAP expression, specifically in the distal convoluted and connecting tubules. Angiotensin II infusion led to marked blood pressure elevation in wild-type mice, whereas DT-ATRAP TGM showed significantly blunted hypertensive responses. Results from the diuretic test revealed that the amiloride-induced suppression of ENaC activity was greater in WT mice than in DT-ATRAP TGM during angiotensin II stimulation. Transcriptomic analysis is currently ongoing to elucidate ATRAP-regulated signaling cascades in distal tubular cells.
Our data support that ATRAP in the distal nephron protects against angiotensin II–induced hypertension, likely by restraining ENaC. A more comprehensive understanding of ATRAP-mediated transcriptional regulation of ENaC may uncover new therapeutic strategies targeting segment-specific intrarenal RAS control in hypertension.
