Regulates central hypertension through its calcium-modulated preference to cleave N-terminal acidic residues from peptides such as angiotensin II. Release of N-terminal glutamate (and to a lesser extent aspartate) from a peptide. Binds 1 zinc ion per subunit. Substrate specificity is modulated by calcium which enhances the enzymatic activity for cleavage of acidic residues while reducing its activity with basic residues. Inhibited by aminopeptidase inhibitors amastatin and bestatin. Homodimer; disulfide-linked. Highest expression in kidney proximal tubules and ileum enterocytes. High expression also detected in liver and pituitary. Lower levels in heart, adrenal gland and brain. Not detected in aorta, lung or spleen. In heart, higher levels in ventricle than in atrium. Also expressed in glomerular mesangial cells. Belongs to the peptidase M1 family.