AHA CDA 11/1/2019 - 10/31/2022

Raw patch-clamp data over the years of work on AHA Career Development Award on the topic of "Importance of collecting duct ClC-Kb/2 channel for urinary electrolyte excretion"
Overall, I demonstrated that ClC-K2/b function in the ICs is primarily regulated by dietary Cl- intake in an Ang II-dependent manner. Transcellular ClC-K2/b-mediated Cl- flux reduces the ENaC-generated driving force for K+ secretion (see Principal Scheme) switching the CD transport profile from Na+/K+ exchange during hyperkalemia (only aldosterone is elevated) to NaCl reabsorption during hypovolemia (both aldosterone and Ang II are high). Overstimulation of ENaC and ClC-K2/b by chronically elevated Ang II causes renal salt conservation contributing to Ang II-induced hypertension.