Role of glomerular nitric oxide in glycerol-induced acute renal failure

Myoglobinuric acute renal failure remains one of the least understood clini cal syndromes and the mediators involved remain obscure. The aim of the pre sent study was to assess the role of nitric oxide in glycerol-induced acute renal failure under normal conditions and after uninephrectomy. Acute rena l failure was induced in rats by injection of 50% glycerol (10 mL.kg(-1) bo dy weight). Half of the animals were subjected to uninephrectomy two days b efore glycerol injection. Two days after the induction of acute renal failu re, glomeruli from some animals were isolated and glomerular nitrite produc tion was measured. Another group of animals was used for acute clearance st udies. In this case, the effect of infusing either L-NAME or L-arginine was assayed. Glomerular nitrite production was significantly decreased in glyc erol-induced acute renal failure. Glomeruli from uninephrectomized animals showed an increase in nitrite production, both in normal conditions and aft er glycerol injection, as compared with glomeruli from non-nephrectomized a nimals. L-NAME infusion worsened renal function in all the study groups, bu t more slowly in animals with glycerol-induced acute renal failure than in control rats. In uninephrectomized animals L-NAME reduced renal function mo re than in animals with two kidneys. In conclusion in this model of acute r enal failure the decrease in glomerular nitric oxide production plays an im portant role in the decrease in renal function. After uninephrectomy, an in crease in glomerular nitric oxide synthesis plays a protective role against glycerol-induced acute renal failure.