PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30716330-10 2019 Also, combined blockade of COX and neuronal NOS (nNOS) blunted acetylcholine-induced vasodilation, while combined COX and inducible NOS (iNOS) inhibition had no effect. Acetylcholine 63-76 nitric oxide synthase 1, neuronal Mus musculus 35-47 9150796-6 1997 These data suggest that type II NMJ are provided with additional regulatory mechanisms, such as free radical signaling by the NOS I-derived NO which may exert modulatory effects on the choline acetyltransferase/ACh/AChE pathway. Acetylcholine 211-214 nitric oxide synthase 1, neuronal Mus musculus 126-131 8853353-0 1996 ACh dilates pial arterioles in endothelial and neuronal NOS knockout mice by NO-dependent mechanisms. Acetylcholine 0-3 nitric oxide synthase 1, neuronal Mus musculus 47-59 8853353-8 1996 Our findings indicate that 1) ACh dilates pial arterioles of wild-type mice by NOS-dependent mechanisms as reported in other species, 2) the response in nNOS mutant mice resembles the wild-type response except for enhanced dilation to ACh and reduced L-NNA sensitivity, and 3) surprisingly, the response in eNOS mutant mice is partially NOS dependent and attenuated by both TTX and L-NNA. Acetylcholine 235-238 nitric oxide synthase 1, neuronal Mus musculus 153-157 8996510-1 1997 BACKGROUND AND PURPOSE: Tetrahydrobiopterin (THBP) is an essential cofactor for nitric oxide synthase (NOS), which is responsible for the synthesis of the endothelium-derived relaxing factor (EDRF) responsible for mediating the vasorelaxation produced by acetylcholine (ACh). Acetylcholine 255-268 nitric oxide synthase 1, neuronal Mus musculus 80-101 8996510-1 1997 BACKGROUND AND PURPOSE: Tetrahydrobiopterin (THBP) is an essential cofactor for nitric oxide synthase (NOS), which is responsible for the synthesis of the endothelium-derived relaxing factor (EDRF) responsible for mediating the vasorelaxation produced by acetylcholine (ACh). Acetylcholine 270-273 nitric oxide synthase 1, neuronal Mus musculus 80-101 30716330-10 2019 Also, combined blockade of COX and neuronal NOS (nNOS) blunted acetylcholine-induced vasodilation, while combined COX and inducible NOS (iNOS) inhibition had no effect. Acetylcholine 63-76 nitric oxide synthase 1, neuronal Mus musculus 49-53 27435231-9 2016 Inhibition of NO synthase (NOS) activity or H2O2 decomposition by catalase abolished the differences in the acetylcholine response between the animals. Acetylcholine 108-121 nitric oxide synthase 1, neuronal Mus musculus 14-25 30105819-10 2018 In WT and cav-1 KO, dilation to ACh was enhanced by MO through increased role for NOS and cyclooxygenase. Acetylcholine 32-35 nitric oxide synthase 1, neuronal Mus musculus 82-104 29183804-7 2018 We demonstrate here that acetylcholine (Ach)-induced relaxation is completely abolished by nNOS inhibition in eNOS silenced mice aorta which also decreased NO and H2O2 concentrations. Acetylcholine 25-38 nitric oxide synthase 1, neuronal Mus musculus 91-95 29183804-7 2018 We demonstrate here that acetylcholine (Ach)-induced relaxation is completely abolished by nNOS inhibition in eNOS silenced mice aorta which also decreased NO and H2O2 concentrations. Acetylcholine 40-43 nitric oxide synthase 1, neuronal Mus musculus 91-95 28503149-12 2017 Taken together, our findings show that B1- and B2-kinin receptors regulate the endothelium-dependent vasodilation of ACh through nNOS activity and indicate that molecular disturbance of short-range interaction between B1- and B2-kinin receptors with nNOS might be involved in the oxidative pathogenesis of endothelial dysfunction. Acetylcholine 117-120 nitric oxide synthase 1, neuronal Mus musculus 129-133 28503149-12 2017 Taken together, our findings show that B1- and B2-kinin receptors regulate the endothelium-dependent vasodilation of ACh through nNOS activity and indicate that molecular disturbance of short-range interaction between B1- and B2-kinin receptors with nNOS might be involved in the oxidative pathogenesis of endothelial dysfunction. Acetylcholine 117-120 nitric oxide synthase 1, neuronal Mus musculus 250-254 26444418-4 2016 As in non-atherosclerotic conditions, the muscarinic receptor agonist acetylcholine (ACh) evoked an endothelium-dependent, COX-mediated contraction following NO synthase (NOS) inhibition in abdominal aortic rings from atherosclerotic apoE(-/-) mice. Acetylcholine 70-83 nitric oxide synthase 1, neuronal Mus musculus 158-169 26976926-8 2016 Selective inhibition of nNOS and catalase led to a higher reduction in the effect of ACh in sham than in DOCA-salt-hypertensive mice. Acetylcholine 85-88 nitric oxide synthase 1, neuronal Mus musculus 24-28 26444418-4 2016 As in non-atherosclerotic conditions, the muscarinic receptor agonist acetylcholine (ACh) evoked an endothelium-dependent, COX-mediated contraction following NO synthase (NOS) inhibition in abdominal aortic rings from atherosclerotic apoE(-/-) mice. Acetylcholine 85-88 nitric oxide synthase 1, neuronal Mus musculus 158-169 21615722-9 2011 Inhibition of nNOS with L-Arg(NO2) -L-Dbu, knockdown of nNOS and catalase, which decomposes H(2)O(2) into oxygen and water, decreased ACh-induced relaxation by half, produced a small diminution of NO production and abolished H(2)O(2) in wild-type animals, but had no effect in ApoE(-/-) mice. Acetylcholine 134-137 nitric oxide synthase 1, neuronal Mus musculus 14-18 23709593-4 2013 Dilation to acetylcholine at P7 was abolished by inhibition of NO synthase (NOS) (l-NAME) or of phosphoinositide-3-kinase (PI3K) (wortmannin, LY294002). Acetylcholine 12-25 nitric oxide synthase 1, neuronal Mus musculus 63-74 23818850-4 2013 We show that pial arteriolar responses to endothelial NOS (eNOS) and neuronal NOS (nNOS) agonists (Acetylcholine (ACh) and N-Methyl-D-Aspartate (NMDA)) were blunted in mice with ECM, and could be partially recovered by exogenous supplementation of tetrahydrobiopterin (BH4). Acetylcholine 99-112 nitric oxide synthase 1, neuronal Mus musculus 83-87 22580898-5 2012 Leptin also sensitized aortae from eNOS(-/-) mice to acetylcholine, an effect blocked by neuronal NOS (nNOS) inhibition and not observed in eNOS-nNOS double(-/-) mice. Acetylcholine 53-66 nitric oxide synthase 1, neuronal Mus musculus 89-101 21615722-9 2011 Inhibition of nNOS with L-Arg(NO2) -L-Dbu, knockdown of nNOS and catalase, which decomposes H(2)O(2) into oxygen and water, decreased ACh-induced relaxation by half, produced a small diminution of NO production and abolished H(2)O(2) in wild-type animals, but had no effect in ApoE(-/-) mice. Acetylcholine 134-137 nitric oxide synthase 1, neuronal Mus musculus 56-60 20624383-8 2010 Selective pharmacological inhibition of nNOS with L-Arg(NO2)-L-Dbu-NH(2) 2TFA and specific knock-down of nNOS abrogated H(2)O(2) and decreased by half acetylcholine-induced vasodilation. Acetylcholine 151-164 nitric oxide synthase 1, neuronal Mus musculus 40-44 20624383-8 2010 Selective pharmacological inhibition of nNOS with L-Arg(NO2)-L-Dbu-NH(2) 2TFA and specific knock-down of nNOS abrogated H(2)O(2) and decreased by half acetylcholine-induced vasodilation. Acetylcholine 151-164 nitric oxide synthase 1, neuronal Mus musculus 105-109 20624383-11 2010 In eNOS knocked-down mice, pharmacological nNOS inhibition dramatically reduced H(2)O(2) production and further reduced the residual acetylcholine-induced vasodilation. Acetylcholine 133-146 nitric oxide synthase 1, neuronal Mus musculus 43-47 18952716-5 2008 In mice aorta rings, ACh-induced relaxation was inhibited by L-NAME and Nomega-nitro-L-arginine (L-NNA), two nonselective inhibitors of NOS, and attenuated by selective inhibition of nNOS with L-ArgNO2-L-Dbu-NH2 2TFA (L-ArgNO2-L-Dbu) and 1-(2-trifluoromethylphehyl)imidazole (TRIM). Acetylcholine 21-24 nitric oxide synthase 1, neuronal Mus musculus 183-187 20056676-3 2010 Age-dependent hypersensitivity to acetylcholine is abolished by inhibition of nitric oxide synthase (NOS) activity, indicating that Col4a1 mutations affect vasorelaxation mediated by endothelium-derived nitric oxide (NO). Acetylcholine 34-47 nitric oxide synthase 1, neuronal Mus musculus 78-99 18952716-11 2008 Antisense knockdown of nNOS decreased both ACh-dependent relaxation and ACh-induced H2O2 production. Acetylcholine 43-46 nitric oxide synthase 1, neuronal Mus musculus 23-27 18952716-11 2008 Antisense knockdown of nNOS decreased both ACh-dependent relaxation and ACh-induced H2O2 production. Acetylcholine 72-75 nitric oxide synthase 1, neuronal Mus musculus 23-27 17138723-4 2007 Inhibition of nitric oxide synthase (NOS) with N(G) monomethyl L-arginine (L-NMMA) significantly reduced resting diameters and reduced responses to ACh (by 45-63%) in NS mice but not in HS mice. Acetylcholine 148-151 nitric oxide synthase 1, neuronal Mus musculus 14-35 16385082-6 2006 In sham controls, ACh induced dose-dependent vasodilation that was blocked by the nitric oxide synthase (NOS) inhibitor L-NMMA (10 micromol/L), suggesting a key role for NO. Acetylcholine 18-21 nitric oxide synthase 1, neuronal Mus musculus 82-103 11009479-8 2000 In contrast, trifluoromethylphenylimidazole, an inhibitor of neuronal NOS (nNOS), decreased ACh-induced dilation in arteries from eNOS-deficient mice but had no effect on responses in wild-type mice. Acetylcholine 92-95 nitric oxide synthase 1, neuronal Mus musculus 61-73 11009479-8 2000 In contrast, trifluoromethylphenylimidazole, an inhibitor of neuronal NOS (nNOS), decreased ACh-induced dilation in arteries from eNOS-deficient mice but had no effect on responses in wild-type mice. Acetylcholine 92-95 nitric oxide synthase 1, neuronal Mus musculus 75-79