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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.
Acute renal failure with severe loin pain and patchy renal ischemia after high-intensity exercise (ALPE) is a unique form of acute kidney injury. Although heterogeneous renal vasoconstriction has been implicated, its molecular mechanism remains unclear. Arginine Vasopressin (AVP) have a potent vasoconstrictor acting through the AVP receptor 1A (AVPR1A). This study aimed to clarify whether exercise augments AVP-induced renal vasoconstriction and hypoxia via AVPR1A signaling.
Male mice underwent brief high-intensity treadmill running (22 m/min, 1 min) followed by intravenous vasopressin (0.03 µg/g). Continuous recordings of mean arterial blood pressure, mean renal venous pressure, and renal arterial blood flow were obtained to calculate renal vascular resistance. Renal hypoxia was assessed by in vivo bioluminescence imaging using hypoxia-reporter (ODD-Luc) mice and by pimonidazole staining. The selective AVPR1A antagonist SR49059 (10 µg/g i.v.) was administered to test receptor specificity.
Treadmill-primed mice exhibited a rapid fall in renal arterial blood flow and a rise in renal vascular resistance after vasopressin injection, whereas mean arterial blood pressure changes were comparable between groups. Pimonidazole staining revealed stronger corticomedullary-predominant hypoxia in the treadmill group than in the vasopressin-only group. In vivo imaging demonstrated sustained renal hypoxia for 24–48 hours in treadmill-primed mice. Pretreatment with SR49059 abolished or markedly attenuated these hemodynamic and hypoxic changes, confirming AVPR1A-mediated vasoconstriction.
Short high-intensity exercise enhances AVPR1A-dependent renal vasoconstriction and prolongs renal hypoxia, providing a mechanistic explanation for exercise-induced acute kidney injury such as ALPE. Pharmacological AVPR1A blockade may represent a potential therapeutic strategy for preventing exercise-related renal ischemia.
