ACE is present on the luminal surface of vascular endothelia throughout the body and is abundantly present in the **endothelium-rich lungs**.
ACE in the kidney—particularly in the endothelial cells of the afferent and efferent arterioles— can produce enough ANG II to exert local vascular effects.
Thus, the kidney _receives_ ANG II from two sources:
Systemic ANG II comes from the general circulation and originates largely from the pulmonary region, and
Local ANG II forms from the renal conversion of systemic ANG I.
• In addition, the proximal tubule **secretes** ANG II into its lumen and thus achieves intraluminal concentrations in excess of those in the general circulation. ANG II in the circulation has a short half-life (~2 min).