These findings suggest that CaCC TMEM16A modulates the vasocontractility of basilar arteries of 2K2C renal hypertensive rats; however, in sharp contrast with SHRs, the activity of CaCCs was decreased gradually during the development of hypertension, and the CaCCs’ current density was negatively correlated with blood pressure levels, in basilar arteries of 2K2C renal hypertensive rats [60] (Table 1). The gene discussed is ANO1; the disease is hypertensive disorder.