POS-274 Deletion of Kir4.1 prevents salt-sensitive hypertension in streptozotocin-induced diabetic mice via sodium-chloride cotransporter in the distal convoluted tubule

Salt-sensitive hypertension is one of the common complications in diabetes mellitus, accompanied by upregulation of Na+-Cl-cotransporter (NCC), a major sodium transporter targeted by thiazide diuretics in the distal convoluted tubule (DCT). Basolateral Kir4.1/Kir5.1 heterotetramer plays an important role in the regulation of NCC activity through a Cl--sensitive WNK-SPAK pathway. We hypothesized that Kir4.1 deficiency mitigates high salt intake-induced increase in blood pressure in type 1 diabetic mice through compromising NCC function.