These studies have informed us that the responses of sodium transporters to acute AngII are distinct from the responses to chronic AngII: acutely, both proximal tubule NHE3 and distal tubule NCC redistribute into domains of apical membranes where they are active (without changes in abundance or phosphorylation); during chronic AngII infusion, with accompanying hypertension, the abundance of proximal NHE3 in the apical membrane is depressed, whereas abundance and phosphorylation of distal NCC in apical membranes is increased. Here, SLC9A3 is linked to hypertensive disorder.