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

Abstract

Myoglobinuric acute renal failure remains one of the least understood clinical syndromes and the mediators involved remain obscure. The aim of the present study was to assess the role of nitric oxide in glycerol-induced acute renal failure under normal conditions and after uninephrectomy. Acute renal failure was induced in rats by injection of 50% glycerol (10 mL x kg(-1) body weight). Half of the animals were subjected to uninephrectomy two days before glycerol injection. Two days after the induction of acute renal failure, glomeruli from some animals were isolated and glomerular nitrite production was measured. Another group of animals was used for acute clearance studies. In this case, the effect of infusing either L-NAME or L-arginine was assayed. Glomerular nitrite production was significantly decreased in glycerol-induced acute renal failure. Glomeruli from uninephrectomized animals showed an increase in nitrite production, both in normal conditions and after glycerol injection, as compared with glomeruli from non-nephrectomized animals. L-NAME infusion worsened renal function in all the study groups, but more slowly in animals with glycerol-induced acute renal failure than in control rats. In uninephrectomized animals L-NAME reduced renal function more than in animals with two kidneys. In conclusion, in this model of acute renal failure the decrease in glomerular nitric oxide production plays an important role in the decrease in renal function. After uninephrectomy, an increase in glomerular nitric oxide synthesis plays a protective role against glycerol-induced acute renal failure.

L-Carnitine Ameliorates Glycerol-Induced Myoglobinuric Acute Renal Failure in Rats

“…[24] Reduced bioavailable NO, a potent renal vasodilatator, can contribute to renal vasoconstriction/hypoperfusion and tissue injury in the setting of myoglobinuric ARF. [25] L-carnitine treatment may lead to a reduction of NO inactivation by ROS with enhanced NO bioavailability. Recently, it has been reported that L-carnitine was able to improve the endothelium-dependent relaxation of small mesenteric arteries from SHR by decreasing vascular O 2 − production, thus increasing NO participation in endothelial function.…”

Experimental Myoglobinuric Acute Renal Failure: The Effect of Vitamin C

“…[30] Reduced bioavailable nitric oxide (NO), a potent renal vasodilatator, can contribute to renal hypoperfusion and tissue injury in the setting of myoglobinuric ARF. [31] It has been shown that vitamin C improves NO bioavailability and NO-mediated resistance vessel dilatation. [32] This molecular mechanism provides potential renoprotective capacity through the inhibition of renal vasoconstriction in myoglobinuric ARF.…”

Effects of Short- and Long-Term Hypercholesterolemia on Contrast-Induced Acute Kidney Injury

“…The NO levels in the cortex were represented by the concentration of nitrate and nitrite (NO x ) in the cortex, as suggested by Valdivielso et al [12]. The cortical nitrate was reduced to nitrite by nitrate reductase.…”