Background. In the neonatal period, angiotensin II (Ang II) is up-regulated
and induces a timely development of the renal pelvis and ureteral peristal
sis, thereby protecting the kidney from hydronephrosis. We tested the possi
bility that in adulthood, Ang II may act salutarily on the kidney structure
during partial urinary tract obstruction by inducing adaptive changes in t
he peristaltic machinery.
Methods. Adult male Sprague-Dawley rats were subjected to partial unilatera
l ureteral obstruction (UUO) and divided into two groups, that is, those tr
eated with (group L, N = 21) and those without (group C, N = 21) an angiote
nsin type 1 (AT1) receptor antagonist (losartan). Control animals were sham
operated (N = 10). Rats were sacrificed either at day 7 or day 14.
Results. The degree of hydronephrosis determined morphometrically was signi
ficantly more severe in group L than group C at both day 7 and day 14, indi
cating that Ang II inhibition accentuated hydronephrosis. The measurement o
f upstream pressure within the partially ligated ureter in vivo revealed th
at losartan significantly attenuates the frequency of ureteral peristaltic
activities. In in vitro studies using ureteral strips harvested from normal
adult Sprague-Dawley rats (N = 10), Ang II (10(-8) mol/L) was shown to aug
ment contraction, which was completely inhibited by losartan (10(-6) mol/L)
.
Conclusions. Ang II has a salutary effect of protecting kidneys from hydron
ephrosis during partial ureteral obstruction through its ability to augment
ureteral peristalsis.