L-NAMEG -nitro-L-Arginine-Methyl Ester
L-NAMEL-Nitro-Arginine Methyl Ester
L-NAMEN-Nitro-L-Arginine Methyl Ester
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The rats in the L-NAME group were treated with L-NAME (Cayman Chemical Company, Ann Arbor, MI, USA; 1 mg/mL) in their drinking water for 8 weeks (the water was replaced daily).
To confirm the involvement of eNOS in modulation of Ang (1-7)-dependent antiapoptotic effect, studies were carried out in the presence of the specific eNOS inhibitor L-NAME. L-NAME had no noticeable effects on cellular apoptosis but prevented the ability of Ang (1-7) to suppress apoptosis induced by palmitate (P < 0.05) (Figure 4(c)).
At the age of 4 weeks, half the animals were given a subpressor dose of L-NAME (5mg/L), an inhibitor of NOS, in the drinking water (Sigma-Aldrich Cat number N5751).
To confirm that the effect of ASA on macrophage activity depends on [NO.sup.*] levels, we assessed the entry of trypomastigotes into macrophages incubated with aminoguanidine (AG, iNOS inhibitor) or with L-NAME (cNOS inhibitor).
delayed circulatory failure following endotoxic shock in rats and improves survival.10 AG and L-NAME improve the survival rate following
L-NAME in combination with DECC did not change the negative inotropy, negative chronotropy and the decrease in coronary flow induced by DECC.
To further assess the involvement of EDNO and prostacyclin ([PGI.sub.2]) releases, relaxations of aortic rings were performed in WOS, WMOS, and losartan groups preincubated for 30 minutes with L-NAME (100 [micro]M), a nonspecific NO synthase inhibitor, and indomethacin (10 [micro]M), a nonselective cyclooxygenase inhibitor, respectively.
L-NAME potentiated the antidepressant action of the sub-effective dose of bilberry extract (250 mg/kg).
Using this economically important animal model, the objectives of present study were: i) to verify NO effect using SNP (NO donor) on steroid synthesis, growth and apoptosis in GC ii) to verify whether the effects of SNP are modulated by L-NAME (NOS inhibitor) and heamoglobin (NO scavenger).