In hypertension caused by unilateral renal artery stenosis, the nonste
notic kidney becomes renin depleted but fails to prevent hypertension.
The nonstenotic kidney mysteriously develops elevated infrarenal angi
otensin II (ANG II) content. Rats chronically infused with ANG II exhi
bit a similar hypertensive process. The augmentation of intrarenal ANG
II is due to receptor-mediated internalization and continued ANG II f
ormation, which provide a hypertensinogenic stimulus.