Taken together, these findings suggest that upregulation of endothelial CaCC TMEM16A may contribute to the impaired endothelial function, and if so, that it likely does so via a reduction in the activity of EDH and/or NO; finally, the results suggest that such a reduction in EDH and/or NO activity may be at least partly responsible for the elevated blood pressure in hypertension (Figure 3). Here, ANO1 is linked to Hypertension.