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Abstract

Although it is the smallest segment of the nephron, the distal convoluted tubule (DCT) plays an outsized role in electrolyte homeostasis through regulation of several ions, including sodium. In the DCT, sodium balance is primarily determined by the regulation of the sodium-chloride cotransporter (NCC). When phosphorylated, NCC reabsorbs sodium away from the lumen of the nephron. Dephosphorylation of NCC inactivates this reabsorption resulting in increased sodium excretion. A similar effect is leveraged by a common class of anti-hypertensive medications called thiazides, which block NCC activity. Gaining a better understanding of the molecular mechanism by which NCC is regulated holds high clinical relevance to several diseases including hypertension, FHHt, and Gitelman syndrome. To investigate a novel mechanism that may regulate NCC activity, we implemented a cell-specific chemogenetic approach with Designer Receptors Exclusively Activated by Designer Drugs (DREADD) technology.

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