L-NAME HCl

NO-mediated neurotoxicity is induced by reaction with superoxide (O^2-), leading to formation of neurotoxic substance, peroxynitrite (ONOO) (Radi et al., 1991). We (Abekawa et al., 1996) have shown that a high dose of a non-selective eNOS and nNOS inhibitor, L-NAME (30mg/kg, i.p., 2) significantly reduced the METH-induced decreases in contents of dopamine and its metabolites in the striatum. Consistent with our report, several groups revealed that not only high doses of L-NAME (37, 75, 150, and 300mg/kg 2) but also high doses of a nNOS selective NOS inhibitor, 7-NI (25mg/kg 3 or 50mg/kg 4) attenuated the METH-induced dopaminergic neurotoxicity in the striatum of mice (Di Monte et al., 1996; Itzhak and Ali, 1996; Taraska and Finnegan, 1997). Recently, Itzhak et al. (1998) reported that nNOSdeficient mice were resistant to the METH-induced neurotoxicity. These findings suggest that the METH-induced dopaminergic neurotoxicity is mediated by nNOS-producing NO.

Nitric oxide is involved in the regulation of corpus luteum (CL) function and life span depending on the stage of CL development (Motta et al. 2001). At the early stage of CL development, nitric oxide promotes progesterone production (Tamanini et al. 2003), but at mid and late luteal phase, it inhibits progesterone production. Nitric oxide is a potent luteolytic agent synthesized in the body from L-arginine through the action of enzyme nitric oxide synthase. The formation of nitric acid is an oxygen and NADPHdependant reaction. There are several drugs like 7-nitro indazole (Ivana et al. 2002), N-phenylamidines (Suaifan et al. 2010) and L-arginine methyl ester (L-NAME) (Dariusz et al. 2003) which inhibit the nitric oxide concentration by checking the nitric oxide synthase enzyme. The involvement of L-NAME for PGF-induced luteolysis has been documented in cattle (Dariusz et al. 2003), but the studies are lacking in buffaloes. The objective of the present study was to evaluate the effect of L-NAME administration on the blood serum concentrations of progesterone and estrogen, the life span of the CL and the length of the estrous cycle in buffaloes.

Significant alterations of methyl cycle metabolites were observed under action of L-NAME. It was found that the content of SAM in MCR cells in the presence of L-NAME was increased, whereas the synthesis of SAM in the MVR cells was greatly reduced. And vice versa, in the MCR cells accumulation of SAM under action of L-NAME was decreased, while the production of SAH significantly rose. These opposite changes showed that MVR cells differ from MCR on sensitivity to constitutional levels of nitric oxide, that apparently act on the oncogenic and normal Ras by distinct ways.

The present study assessed whether dynamic MRI is a suitable method for measuring changes in renal function in a rat model with acute hypertension in response to the nitric oxide (NO) synthase inhibitor NG-nitro-l-arginine methylester (l-NAME). Nitric oxide (NO) is an endothelium-dependent vasodilatorwhichissynthesizedinresponsetovariousstimuli, and when released at the vicinity of glomeruli, increases blood flow resulting in increased GFR and urine formation. Inhibiting NO synthesis with l-NAME leads to an increase in blood pressure through vasoconstriction of vascular smooth muscle cells and reduction in renal blood flow, which leads to decreased GFR and sodium excretion.