Abstract
The distal convoluted tubule (DCT) plays a central role in blood pressure and potassium homeostasis, as evidenced by diseases that occur when its function is modified. The paper by van der Lubbe and colleagues makes clear that angiotensin II itself increases the activity and abundance of the thiazide-sensitive Na-Cl cotransporter (NCC), independent of changes in circulating aldosterone. This Commentary provides additional perspective on that work.