and widening and thickening of infrarenal arterial vessels' [72]. The third SNP, H66R, is in chymase (CMA1), and changes a key catalytic residue, as well a breaking a salt bridge. The physiological function of chymase is still controversial [73,74]. A SNP upstream of the transcription initiation site of CMA1 has been reported to be associated with hypertensive complications such as HDL cholesterol (possibly related to its lipid metabolism function), but not with blood pressure [75]. The fourth SNP, V193E, in kallikrein (KLK1) results in a buried charge and loss of hydrophobic burial, affecting bradykinin processing.
