In addition, they explained that the mechanism of ACEi- and ARB-induced hyponatremia has not been confirmed, but ACEi therapy increased the circulating angiotensin I that enters the brain and is converted into angiotensin II, which may stimulate thirst and release of antidiuretic hormone from the hypothalamus, eventually leading to hyponatremia [22, 23]. This evidence concerns the gene AGT and Hyponatremia.