PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 7706486-8 1995 Indeed, sodium nitroprusside, a NO donor, decreased and L-NAME (N-nitro-L-arginine methyl ester), an inhibitor of NO-synthesis, increased both VEGF and VEGF receptor transcripts. NG-Nitroarginine Methyl Ester 56-62 vascular endothelial growth factor A Rattus norvegicus 152-156 30119970-10 2018 VEGF and PIGF levels were decreased in the L-NAME administered rats, while this levels were increased in the L-NAME + L-Arg group and L-Arg group when compared with the L-NAME alone group (p < 0.05). NG-Nitroarginine Methyl Ester 43-49 vascular endothelial growth factor A Rattus norvegicus 0-4 31486114-10 2019 In short, the present study suggests that the inhibition of placental TFPI-2 and HIF-1alpha/VEGF might be one of the potential mechanisms underlying the protective effects of VI to experimental PE induced by l-NAME. NG-Nitroarginine Methyl Ester 208-214 vascular endothelial growth factor A Rattus norvegicus 92-96 24278109-8 2013 In the L-NAME model, several factors involved in alveolarization, VEGF, VEGF-R1 and -R2, MMP14, MMP16, FGFR3 and 4, FGF18 and 7, were significantly decreased at day 4 and/or day 10, while the various factors studied were not modified in the LPD group. NG-Nitroarginine Methyl Ester 7-13 vascular endothelial growth factor A Rattus norvegicus 66-70 28078001-9 2016 In contrast, the L-NAME treatment reduced the expression of VEGF and increased the expression of endostatin. NG-Nitroarginine Methyl Ester 17-23 vascular endothelial growth factor A Rattus norvegicus 60-64 27856999-5 2017 In addition, dams from the l-NAME group showed lower vascular endothelial growth factor (VEGF) and interleukin (IL) 10 levels and higher plasma-soluble FMS-like tyrosine kinase 1 (sFlt-1), tumor necrosis factor alpha (TNF-alpha), and oxidative stress marker malondialdehyde (MDA) levels as compared to control dams ( P < .01, for all). NG-Nitroarginine Methyl Ester 27-33 vascular endothelial growth factor A Rattus norvegicus 53-87 27856999-5 2017 In addition, dams from the l-NAME group showed lower vascular endothelial growth factor (VEGF) and interleukin (IL) 10 levels and higher plasma-soluble FMS-like tyrosine kinase 1 (sFlt-1), tumor necrosis factor alpha (TNF-alpha), and oxidative stress marker malondialdehyde (MDA) levels as compared to control dams ( P < .01, for all). NG-Nitroarginine Methyl Ester 27-33 vascular endothelial growth factor A Rattus norvegicus 89-93 27638877-6 2016 VEGFA-induced relaxations were also inhibited in endothelial-denuded arteries and in arteries pretreated with the nitric oxide synthase (NOS) inhibitor, Nomega-nitro-l-arginine methyl ester (100 muM). NG-Nitroarginine Methyl Ester 153-189 vascular endothelial growth factor A Rattus norvegicus 0-5 24344561-9 2013 Premedication with ZM323881 or L-NAME decreased the dilatory effects of VEGF. NG-Nitroarginine Methyl Ester 31-37 vascular endothelial growth factor A Rattus norvegicus 72-76 21969195-9 2011 The eNOS protein expression and NO production were significantly increased from 72 to 168 h. The expression of VEGF protein was significantly increased at 72 h. L-NAME significantly inhibited the increases in the liver mass and decreased the PCNA labeling index of hepatocytes at 24 h. L-NAME also inhibited the induction of VEGF protein at 72 h. CONCLUSIONS: Endothelial NOS and VEGF coordinately regulate SEC proliferation during liver regeneration. NG-Nitroarginine Methyl Ester 161-167 vascular endothelial growth factor A Rattus norvegicus 111-115 23649256-4 2013 VEGF mRNA expression was temporally decreased by L-NAME, but recovered to normal levels after 24 h of treatment, whereas hypoxia inducible factor (HIF)-1alpha and induced NOS (iNOS) expression increased. NG-Nitroarginine Methyl Ester 49-55 vascular endothelial growth factor A Rattus norvegicus 0-4 23649256-5 2013 VEGF expression decreased significantly in placental explants after 6 h of co-treatment with L-NAME and lipopolysaccharide, an iNOS inducer. NG-Nitroarginine Methyl Ester 93-99 vascular endothelial growth factor A Rattus norvegicus 0-4 21969195-9 2011 The eNOS protein expression and NO production were significantly increased from 72 to 168 h. The expression of VEGF protein was significantly increased at 72 h. L-NAME significantly inhibited the increases in the liver mass and decreased the PCNA labeling index of hepatocytes at 24 h. L-NAME also inhibited the induction of VEGF protein at 72 h. CONCLUSIONS: Endothelial NOS and VEGF coordinately regulate SEC proliferation during liver regeneration. NG-Nitroarginine Methyl Ester 161-167 vascular endothelial growth factor A Rattus norvegicus 325-329 21969195-9 2011 The eNOS protein expression and NO production were significantly increased from 72 to 168 h. The expression of VEGF protein was significantly increased at 72 h. L-NAME significantly inhibited the increases in the liver mass and decreased the PCNA labeling index of hepatocytes at 24 h. L-NAME also inhibited the induction of VEGF protein at 72 h. CONCLUSIONS: Endothelial NOS and VEGF coordinately regulate SEC proliferation during liver regeneration. NG-Nitroarginine Methyl Ester 161-167 vascular endothelial growth factor A Rattus norvegicus 325-329 21969195-9 2011 The eNOS protein expression and NO production were significantly increased from 72 to 168 h. The expression of VEGF protein was significantly increased at 72 h. L-NAME significantly inhibited the increases in the liver mass and decreased the PCNA labeling index of hepatocytes at 24 h. L-NAME also inhibited the induction of VEGF protein at 72 h. CONCLUSIONS: Endothelial NOS and VEGF coordinately regulate SEC proliferation during liver regeneration. NG-Nitroarginine Methyl Ester 286-292 vascular endothelial growth factor A Rattus norvegicus 111-115 19722804-9 2009 Premedication with ZM323881 or L-NAME decreased the dilatory effects of VEGF. NG-Nitroarginine Methyl Ester 31-37 vascular endothelial growth factor A Rattus norvegicus 72-76 18855264-0 2008 Vascular endothelial growth factor attenuates Nomega-nitro-L-arginine methyl ester-induced preeclampsia-like manifestations in rats. NG-Nitroarginine Methyl Ester 46-82 vascular endothelial growth factor A Rattus norvegicus 0-34 19922391-11 2009 Positive immunoreactivity for vascular endothelial growth factor (VEGF) was observed in cholesterol and cholesterol plus L-NAME plus ANG II. NG-Nitroarginine Methyl Ester 121-127 vascular endothelial growth factor A Rattus norvegicus 30-64 19922391-11 2009 Positive immunoreactivity for vascular endothelial growth factor (VEGF) was observed in cholesterol and cholesterol plus L-NAME plus ANG II. NG-Nitroarginine Methyl Ester 121-127 vascular endothelial growth factor A Rattus norvegicus 66-70 18835919-5 2008 NG-nitro-L-arginine methyl ester (L-NAME) (1x10(-5) M) eliminated vasodilation to flow, VEGF, and ACh, indicating dependence of these responses on NO. NG-Nitroarginine Methyl Ester 0-32 vascular endothelial growth factor A Rattus norvegicus 88-92 18835919-5 2008 NG-nitro-L-arginine methyl ester (L-NAME) (1x10(-5) M) eliminated vasodilation to flow, VEGF, and ACh, indicating dependence of these responses on NO. NG-Nitroarginine Methyl Ester 34-40 vascular endothelial growth factor A Rattus norvegicus 88-92 18855264-1 2008 OBJECTIVES: To verify the hypothesis that vascular endothelial growth factor (VEGF) attenuates Nomega-Nitro-L-arginine Methyl Ester (L-NAME)-induced preeclampsia-like manifestations in rats. NG-Nitroarginine Methyl Ester 95-131 vascular endothelial growth factor A Rattus norvegicus 42-76 18855264-1 2008 OBJECTIVES: To verify the hypothesis that vascular endothelial growth factor (VEGF) attenuates Nomega-Nitro-L-arginine Methyl Ester (L-NAME)-induced preeclampsia-like manifestations in rats. NG-Nitroarginine Methyl Ester 95-131 vascular endothelial growth factor A Rattus norvegicus 78-82 18855264-1 2008 OBJECTIVES: To verify the hypothesis that vascular endothelial growth factor (VEGF) attenuates Nomega-Nitro-L-arginine Methyl Ester (L-NAME)-induced preeclampsia-like manifestations in rats. NG-Nitroarginine Methyl Ester 133-139 vascular endothelial growth factor A Rattus norvegicus 42-76 18855264-1 2008 OBJECTIVES: To verify the hypothesis that vascular endothelial growth factor (VEGF) attenuates Nomega-Nitro-L-arginine Methyl Ester (L-NAME)-induced preeclampsia-like manifestations in rats. NG-Nitroarginine Methyl Ester 133-139 vascular endothelial growth factor A Rattus norvegicus 78-82 18855264-11 2008 CONCLUSION: VEGF attenuates L-NAME-induced preeclampsia-like manifestations in rats, suggesting the important role of VEGF in preeclampsia and providing a potential strategy for the prevention and treatment of preeclampsia. NG-Nitroarginine Methyl Ester 28-34 vascular endothelial growth factor A Rattus norvegicus 12-16 18855264-11 2008 CONCLUSION: VEGF attenuates L-NAME-induced preeclampsia-like manifestations in rats, suggesting the important role of VEGF in preeclampsia and providing a potential strategy for the prevention and treatment of preeclampsia. NG-Nitroarginine Methyl Ester 28-34 vascular endothelial growth factor A Rattus norvegicus 118-122 18085359-6 2008 L-NAME significantly decreased MDA and NO (P < 0.05 vs L-arginine+aortic IR) and increased VEGF (P < 0.05 vs other groups). NG-Nitroarginine Methyl Ester 0-6 vascular endothelial growth factor A Rattus norvegicus 94-98 18622048-11 2008 Likewise, the expression of VEGF was also up-regulated in the colon following DSS treatment, and this response was suppressed by both L-NAME and aminoguanidine. NG-Nitroarginine Methyl Ester 134-140 vascular endothelial growth factor A Rattus norvegicus 28-32 17420770-5 2008 We aimed to determine the effects of L-arginine and NG-nitro-L-arginine methyl ester (L-NAME) on VEGF synthesis and free radicals in a rat model of spinal cord ischemia-reperfusion (IR) injury. NG-Nitroarginine Methyl Ester 52-84 vascular endothelial growth factor A Rattus norvegicus 97-101 17420770-5 2008 We aimed to determine the effects of L-arginine and NG-nitro-L-arginine methyl ester (L-NAME) on VEGF synthesis and free radicals in a rat model of spinal cord ischemia-reperfusion (IR) injury. NG-Nitroarginine Methyl Ester 86-92 vascular endothelial growth factor A Rattus norvegicus 97-101 17420770-12 2008 However, nonselective inhibition of NOS with L-NAME significantly decreased MDA and NO, but increased VEGF levels. NG-Nitroarginine Methyl Ester 45-51 vascular endothelial growth factor A Rattus norvegicus 102-106 17420770-14 2008 CONCLUSION: Nonselective inhibition of NO synthase activity with L-NAME attenuated free radical formation and increased VEGF level when compared with NO precursor L-arginine in a rat model of spinal cord ischemia. NG-Nitroarginine Methyl Ester 65-71 vascular endothelial growth factor A Rattus norvegicus 120-124 12631117-2 2003 We have previously shown that VEGF is up-regulated in a model of chronic cyclosporine (CsA) nephrotoxicity and that l-arginine (l-Arg) improved while N-nitro-l-arginine-methyl ester (L-NAME) worsened fibrosis. NG-Nitroarginine Methyl Ester 183-189 vascular endothelial growth factor A Rattus norvegicus 30-34 16899993-8 2006 In contrast, VEGF expression and RhoA activity was increased in L-NAME-treated animals, and normalized with co-administration of ATO. NG-Nitroarginine Methyl Ester 64-70 vascular endothelial growth factor A Rattus norvegicus 13-17 15708125-10 2005 L-NAME (a NOS inhibitor) reduced the VEGF-increased expression and L-arginine reversed the inhibitory effect of L-NAME. NG-Nitroarginine Methyl Ester 0-6 vascular endothelial growth factor A Rattus norvegicus 37-41 16354548-13 2005 With L-NAME+ VEGF administration, the Ki of the IC became significantly lower than that of the VEGF alone (-38%, p<0.005). NG-Nitroarginine Methyl Ester 5-11 vascular endothelial growth factor A Rattus norvegicus 95-99 16354548-14 2005 Thus, L-NAME produced a much greater decrease in the Ki of the IC in the VEGF treated than the control animals (p<0.05). NG-Nitroarginine Methyl Ester 6-12 vascular endothelial growth factor A Rattus norvegicus 73-77 15191879-10 2004 NG-nitro-L-arginine methyl ester blocked the paracrine effect of hepatocytes or stellate cells on SEC phenotype and blocked the ability of VEGF to preserve the phenotype of SEC cultured alone. NG-Nitroarginine Methyl Ester 0-32 vascular endothelial growth factor A Rattus norvegicus 139-143 15249212-8 2004 Chronic L-NAME administration resulted in a depletion of cardiac NO level, NOS activity, and eNOS, nNOS, and iNOS protein expressions, as well as VEGF gene expression (2-fold increase in VEGF mRNA). NG-Nitroarginine Methyl Ester 8-14 vascular endothelial growth factor A Rattus norvegicus 146-150 15249212-8 2004 Chronic L-NAME administration resulted in a depletion of cardiac NO level, NOS activity, and eNOS, nNOS, and iNOS protein expressions, as well as VEGF gene expression (2-fold increase in VEGF mRNA). NG-Nitroarginine Methyl Ester 8-14 vascular endothelial growth factor A Rattus norvegicus 187-191 12631117-7 2003 VEGF mRNA and protein expressions increased with CsA, further increased with L-NAME and became significantly reduced with L-Arg. NG-Nitroarginine Methyl Ester 77-83 vascular endothelial growth factor A Rattus norvegicus 0-4 12218334-7 2002 In contrast, the number of VEGF-positive smooth muscle cells in the media was greater in the L-NAME group than in the control group. NG-Nitroarginine Methyl Ester 93-99 vascular endothelial growth factor A Rattus norvegicus 27-31 10336886-6 1999 At 4 and 24 h posttreatment, VEGF significantly attenuated thrombin-induced and L-NAME-induced leukocyte rolling, adherence, and transmigration in rat mesenteric venules. NG-Nitroarginine Methyl Ester 80-86 vascular endothelial growth factor A Rattus norvegicus 29-33 11530111-7 2001 In these cells, L-NAME significantly reduced NO synthesis and decreased VEGF generation. NG-Nitroarginine Methyl Ester 16-22 vascular endothelial growth factor A Rattus norvegicus 72-76 11877364-6 2002 We observed vascular inflammation associated with increased VEGF expression within 3 days of L-NAME administration, which was prevented by pretreatment with ACE inhibitor, angiotensin II receptor antagonist, or neutralizing monocyte chemoattractant protein-1 antibody. NG-Nitroarginine Methyl Ester 93-99 vascular endothelial growth factor A Rattus norvegicus 60-64 10749807-8 2000 The exercise-induced increase in VEGF mRNA was attenuated approximately 50% by 30 and 300 mg/kg L-NAME; the TGF-beta(1) mRNA increase was unaffected by 300 mg/kg L-NAME. NG-Nitroarginine Methyl Ester 96-102 vascular endothelial growth factor A Rattus norvegicus 33-37 10712388-9 2000 L-NAME and DAHP totally inhibited NO generation and decreased the IL-1beta-upregulated VEGF synthesis by 30% to 40%. NG-Nitroarginine Methyl Ester 0-6 vascular endothelial growth factor A Rattus norvegicus 87-91 10712388-12 2000 Inhibition of NO generation by L-NAME decreased VEGF synthesis. NG-Nitroarginine Methyl Ester 31-37 vascular endothelial growth factor A Rattus norvegicus 48-52 8761851-10 1996 In addition, pretreatment with N omega-nitro-L-arginine methyl-ester (L-NAME), a nitric oxide (NO) synthase inhibitor, significantly attenuated the depressor and tachycardic responses to VEGF, suggesting that VEGF-induced hypotension may be mediated by NO. NG-Nitroarginine Methyl Ester 31-68 vascular endothelial growth factor A Rattus norvegicus 187-191 8761851-10 1996 In addition, pretreatment with N omega-nitro-L-arginine methyl-ester (L-NAME), a nitric oxide (NO) synthase inhibitor, significantly attenuated the depressor and tachycardic responses to VEGF, suggesting that VEGF-induced hypotension may be mediated by NO. NG-Nitroarginine Methyl Ester 31-68 vascular endothelial growth factor A Rattus norvegicus 209-213 8761851-10 1996 In addition, pretreatment with N omega-nitro-L-arginine methyl-ester (L-NAME), a nitric oxide (NO) synthase inhibitor, significantly attenuated the depressor and tachycardic responses to VEGF, suggesting that VEGF-induced hypotension may be mediated by NO. NG-Nitroarginine Methyl Ester 70-76 vascular endothelial growth factor A Rattus norvegicus 187-191 8761851-10 1996 In addition, pretreatment with N omega-nitro-L-arginine methyl-ester (L-NAME), a nitric oxide (NO) synthase inhibitor, significantly attenuated the depressor and tachycardic responses to VEGF, suggesting that VEGF-induced hypotension may be mediated by NO. NG-Nitroarginine Methyl Ester 70-76 vascular endothelial growth factor A Rattus norvegicus 209-213