Sildenafil and L-NAME
incorporated into the BTS were directly applied to the cavity in a volume of 20 [micro]l.
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).
+ 40 mg/kg p.o.), L-NAME
+ violacein (50 mg/kg i.p.
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
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
delayed circulatory failure following endotoxic shock in rats and improves survival.10 AG and L-NAME
improve the survival rate following
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.
Se uso el modelo de hipertension por L-NAME
, teniendo en cuenta lo realizado por Sanchez-Mendoza y col (15), con modificacion del animal experimental y el sensor para raton, que es usado ampliamente para estudiar la fisiopatologia de la hipertension arterial (16).
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).