While Ang-II-induced hypertension with resulting pressure natriuresis has been suggested as the cause for the increase in urine volume [27], our observation that LCI699 normalized urine volume in dTG rats with little effect on blood pressure indicates that other mechanisms may play a more important role such as impaired renal concentrating ability associated with hyperaldosteronism and hypokalemia [27]. Here, AGT is linked to hyperaldosteronism.