Renal ischemia in the rat stimulates glomerular nitric oxide synthesis

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.