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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.
Sodium–glucose cotransporter 2 inhibitors (SGLT2i), initially developed for glycemic control in type 2 diabetes, have since been shown to exert profound cardiovascular and renal protective effects. The recent FDA approval of the dual SGLT1/2 inhibitor sotagliflozin (Sota) for heart failure with preserved ejection fraction (HFpEF) further underscores the broad therapeutic potential of SGLT inhibition. However, the mechanistic roles of SGLT2 and dual SGLT1/2 inhibition in salt-sensitive hypertension (SS HTN) remain poorly understood. This study aims to elucidate the effects of SGLT inhibition on SS HTN and identify the underlying renal and systemic mechanisms involved.
Eight-week-old Dahl salt-sensitive (SS) rats of both sexes were treated with dapagliflozin (Dapa; 2 mg/kg/day) or sotagliflozin (Sota; 30 mg/kg/day) for three weeks while maintained on a high-salt diet (4% NaCl). In addition, an SGLT2 knockout strain was generated on the Dahl SS background (SSSGLT2-/-). Blood pressure was continuously monitored by radiotelemetry. Comprehensive transcriptomic, proteomic, and lipidomic analyses were performed on renal tissues and biological fluids to elucidate molecular mechanisms of SGLT inhibition.
Our previous studies demonstrated that dapagliflozin (Dapa) prevented the development of salt-sensitive hypertension (SS HTN) in both male and female Dahl SS rats without altering sodium channel expression or the renin–angiotensin–aldosterone system. When administered therapeutically after hypertension was established, Dapa still reduced blood pressure, although the effect was less pronounced. Compared to SGLT2 inhibition, dual SGLT1/2 inhibition produced a greater reduction in mean arterial pressure (MAP; Sota vs. vehicle: 126 ± 2 vs. 157 ± 5 mmHg in males and 126 ± 3 vs. 167 ± 10 mmHg in females), while heart rate (HR) remained unchanged. Under a normal-salt diet (0.4% NaCl), Sota had no effect on MAP or HR. Relative to Dapa, Sota reduced body weight, increased urinary Na⁺ and Cl⁻ excretion, and led to greater fractional glucose excretion. Similarly, genetic deletion of SGLT2 in Dahl SS rats resulted in a significant reduction in blood pressure. Multi-omics analyses of kidneys from SGLT2i-treated animals revealed enrichment of lipid metabolism and inflammatory pathways.
Both genetic and pharmacological inhibition of SGLT2 significantly attenuated blood pressure in Dahl SS rats. Dual SGLT1/2 inhibition produced a more pronounced reduction in salt-sensitive hypertension and renal injury compared to SGLT2 inhibition alone. These findings indicate distinct and potentially additive mechanisms of SGLT1 and SGLT2 modulation, warranting further investigation into the underlying molecular pathways.
