It is not clear why the activity and the expression of CaCC TMEM16A changed in the opposite direction between SHRs and 2K2C renal hypertensive rats, but the difference might be explained by the different levels of activity of the renin–angiotensin system (RAS) in the vasculature: while the plasma and tissue RASs are suppressed in SHRs [61], the RAS components—particularly the vascular Ang II concentration—are increased in 2K2C renal hypertensive rats [62]. Here, ANO1 is linked to hypertensive disorder.