Renal ischemia in humans and in experimental animals is associated with a c
omplex and possibly interrelated series of events. In this study, we have i
nvestigated the glomerular nitric oxide (NO) production after renal ischemi
a. Unilateral or bilateral renal ischemia was induced in Wistar rats by cla
mping one or both renal arteries. NO production was assessed by measuring g
lomerular production of nitrite, a stable end product of NO catabolism, and
NO-dependent glomerular cGMP production and by assessing the glomerular NA
DPH diaphorase (ND) activity, an enzymatic activity that colocalizes with N
O-synthesis activity. Furthermore, we determined the isoform of NO synthase
(NOS) implicated in NO synthesis by Western blot and immunohistochemistry.
Glomeruli from rats with bilateral ischemia showed elevated glomerular nit
rite and cGMP production. Besides, glomeruli from this group of rats showed
an increased ND activity, whereas glomeruli from the ischemic and nonische
mic rats with unilateral ischemia did not show this increase in nitrite, cG
MP, and ND activity. In addition, glomeruli from ischemic kidneys showed an
increased expression of endothelial NOS without changes in the inducible i
soform. Addition of L-NAME in the drinking water induced a higher increase
in the severity of the functional and structural damage in rats with bilate
ral ischemia than in rats with unilateral ischemia and in sham-operated ani
mals. We can conclude that after renal ischemia, there is an increased glom
erular NO synthesis subsequent to an activation of endothelial NOS that pla
ys a protective role in the renal damage induced by ischemia and reperfusio
n.