The present study determined the effect of either occlusion of the left ren
al artery for 60 min (ischemia) or sham operation on angiotensin (ANG) rece
ptors and tissue and urinary levels of ANG peptides between 24 and 72 h rec
overy in male Sprague-Dawley rats. At 24 h postischemia, urinary concentrat
ions of ANG I and ANG-(1-7) rose by an average of 83 and 64%, respectively
(P < 0.05) but had declined to control levels by 72 h. Tissue ANG II rose a
t 24 h in postischemic kidneys by an average of 63% compared with the contr
alateral nonischemic kidney (P < 0.05). Whereas the enzymatic activity of a
ngiotensin-converting enzyme and neprilysin was reduced after ischemia, ren
al renin activity in ischemic kidneys rose by 74% compared with sham-operat
ed kidneys. Receptor autoradiography using I-125-labeled [Sar(1),Thr(8)]ANG
II ( I-125-Sarthran) (0.8 nM) revealed a decreased apparent density of ANG
receptors (>80% AT(1)) in ischemic kidneys with a trend for a decrease in
the contralateral nonischemic kidneys compared with the kidneys from sham-o
perated rats. Twenty-four hours after ischemia, ANG II receptors decreased
by 68% in glomeruli (P < 0.05), 49% in the outer cortical tubulointerstitia
l area (P < 0.05), and 48% in the inner cortical-outer medullary area of th
e vasa recta (P < 0.05). Medullary binding decreased similar to 50% in both
the ischemic kidney and the contralateral nonischemic kidney compared with
sham. In all regions of the ischemic kidney, receptors recovered by 72 h t
o levels not different from sham control rats. The marked change in urinary
ANG I and ANG-(1-7) at 24 h following occlusion indicates these peptides m
ay be potential urinary markers for acute renal ischemia. The reduction of
receptors in vascular and tubular regions of the ischemic kidney provides a
mechanism for the loss of vasoconstrictor responses to ANG II following is
chemia previously reported by others.