Bile Acid–Mediated Regulation of the RAAS–Chloride Axis: Systems Framework with Hypothesis-Generating Clinical and Electrolyte Timing Observations, V 1.6, February 2026

This preprint is Version 1.6 of a technical note series examining mechanistic and systems-level relationships between bile acid signaling, RAAS regulation, and downstream electrolyte balance. Version 1.2 established a mechanistic continuity model linking bile acid receptor signaling to renal nitric oxide production, RAAS modulation, and chloride regulation. Version 1.3 introduced a systems orientation framework describing electrolyte regulation as a continuous regulatory axis linking upstream signaling, renal execution, and downstream electrolyte outcome. Version 1.4 expanded the framework to include hypothesis-generating clinical observations involving bile supplementation and physiological stabilization. Version 1.5 clarified the role of renal nitric oxide and vascular integration as the execution interface linking upstream signaling to downstream electrolyte state. Version 1.6 expands the clinical observation layer to include electrolyte timing and peripheral vascular responses associated with potassium availability and bile-dependent physiological stability. This technical note is hypothesis-generating and intended to support conceptual integration and future controlled investigation.