PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29985945-8 2018 Moreover, ACh-induced relaxation and ACh-stimulated release of NO were significant reduced, associated with suppression of eNOS protein expression in NMPP-treated groups. Acetylcholine 10-13 nitric oxide synthase 3 Homo sapiens 123-127 29985945-8 2018 Moreover, ACh-induced relaxation and ACh-stimulated release of NO were significant reduced, associated with suppression of eNOS protein expression in NMPP-treated groups. Acetylcholine 37-40 nitric oxide synthase 3 Homo sapiens 123-127 12607129-1 2003 OBJECTIVE: Although it has been shown recently that acetylcholine (ACh)-induced vasodilation of forearm resistance vessels is predominantly mediated by nitric oxide, direct biochemical evidence for eNOS stimulation by bradykinin (BK) in the human arterial circulation is still lacking. Acetylcholine 67-70 nitric oxide synthase 3 Homo sapiens 198-202 26273653-3 2015 The effect of Lipofundin MCT/LCT on acetylcholine-induced endothelial nitric oxide synthase (eNOS) phosphorylation in human umbilical vein endothelial cells (HUVECs) was investigated using western blotting. Acetylcholine 36-49 nitric oxide synthase 3 Homo sapiens 58-91 20462865-3 2010 However, it is not entirely clear why activation of eNOS by certain vasodilatory agents, like acetylcholine, does not affect microvascular permeability, whereas activation of eNOS by other inflammatory agents that increase permeability, like platelet-activating factor, does not cause vasodilation. Acetylcholine 94-107 nitric oxide synthase 3 Homo sapiens 52-56 19551451-6 2009 ACh exhibited significant inhibitory effects towards NO, endothelial nitric oxide synthase (eNOS), and IL-1beta secretion especially by tumor cells derived form Duke"s C stage of colon carcinoma. Acetylcholine 0-3 nitric oxide synthase 3 Homo sapiens 57-90 16609365-0 2006 A -786T>C polymorphism in the endothelial nitric oxide synthase gene reduces serum nitrite/nitrate levels from the heart due to an intracoronary injection of acetylcholine. Acetylcholine 161-174 nitric oxide synthase 3 Homo sapiens 33-66 26656861-8 2015 CONCLUSIONS: The results indicated that female sex, diabetes, and mutation in -786T/C eNOS gene correlate with ACh-provoked myocardial ischemia in patients with coronary spasm. Acetylcholine 111-114 nitric oxide synthase 3 Homo sapiens 86-90 19433760-2 2009 However, we recently reported that human forearm basal microvascular tone in vivo is tonically regulated by neuronal NO synthase (nNOS), in contrast to an acetylcholine-stimulated reduction in tone, which is eNOS dependent. Acetylcholine 155-168 nitric oxide synthase 3 Homo sapiens 208-212 19136580-10 2009 ACh failed to stimulate Hsp90-eNOS binding in 2-day-old but induced a significant increase in Hsp90-eNOS coimmunoprecipitation in PRA from the older age groups, which was blocked by Hsp90 antagonism. Acetylcholine 0-3 nitric oxide synthase 3 Homo sapiens 100-104 17977947-0 2008 Diabetic HDL-associated myristic acid inhibits acetylcholine-induced nitric oxide generation by preventing the association of endothelial nitric oxide synthase with calmodulin. Acetylcholine 47-60 nitric oxide synthase 3 Homo sapiens 126-159 17413318-6 2007 The results suggest that increased cerebral expression of NOS3 causes several molecular abnormalities related to AD-type neurodegeneration, including oxidative stress, mitochondrial dysfunction, and impaired acetylcholine homeostasis. Acetylcholine 208-221 nitric oxide synthase 3 Homo sapiens 58-62 12665482-9 2003 Endothelium-dependent and -independent vasodilator responses to acetylcholine and sodium nitroprusside recorded using venous occlusion plethysmography were significantly impaired in patients exhibiting eNOS uncoupling. Acetylcholine 64-77 nitric oxide synthase 3 Homo sapiens 202-206 10409236-4 1999 Acetylcholine-stimulated eNOS activity was 218-255% above basal levels in immortalized cells, and this was comparable to the 250% increase seen in primary PAECs (passage 6). Acetylcholine 0-13 nitric oxide synthase 3 Homo sapiens 25-29 10542298-5 1999 Treatment with oxLDL also inhibited acetylcholine-induced activation of eNOS but not prostacyclin production. Acetylcholine 36-49 nitric oxide synthase 3 Homo sapiens 72-76 11779139-4 2002 On the contrary, activation by acetylcholine or endothelial nitric oxide synthase (eNOS), which produces NO while consuming oxygen, induces a significant decrease in PO(2), whose amplitude is dependent on the acetylcholine dose, i.e., the eNOS activity level. Acetylcholine 31-44 nitric oxide synthase 3 Homo sapiens 48-81 11779139-4 2002 On the contrary, activation by acetylcholine or endothelial nitric oxide synthase (eNOS), which produces NO while consuming oxygen, induces a significant decrease in PO(2), whose amplitude is dependent on the acetylcholine dose, i.e., the eNOS activity level. Acetylcholine 209-222 nitric oxide synthase 3 Homo sapiens 48-81 11434508-2 2001 We tested the hypothesis that the variability in venous response to acetylcholine may be associated with two recently identified genetic polymorphisms for proteins involved in the signal transduction pathway, i.e. the G-protein beta3-subunit (GNB3) and endothelial nitric oxide synthase (eNOS). Acetylcholine 68-81 nitric oxide synthase 3 Homo sapiens 253-286 11434508-2 2001 We tested the hypothesis that the variability in venous response to acetylcholine may be associated with two recently identified genetic polymorphisms for proteins involved in the signal transduction pathway, i.e. the G-protein beta3-subunit (GNB3) and endothelial nitric oxide synthase (eNOS). Acetylcholine 68-81 nitric oxide synthase 3 Homo sapiens 288-292 11132600-13 2000 acetylcholine (average increase: + 554 +/- 371%), nitroprusside or L-NMMA infusion were found across the eNOS genotypes, neither for endothelium-dependent or endothelium-independent vasodilation, nor for basal NO production and release. Acetylcholine 0-13 nitric oxide synthase 3 Homo sapiens 105-109 10694495-2 2000 Under anesthesia, using intravital microscopy and a closed cranial window system, pial arteriolar diameter changes were monitored during sequential cortical suffusions of an eNOS-dependent dilator [acetylcholine (ACh)] and a direct NO donor [S-nitrosoacetylpenicillamine (SNAP)]. Acetylcholine 198-211 nitric oxide synthase 3 Homo sapiens 174-178 31499544-7 2019 The aorta fails to relax completely after the addition of acetylcholine indicates the deranged eNOS signaling in the endothelium. Acetylcholine 58-71 nitric oxide synthase 3 Homo sapiens 95-99 10082505-7 1999 EPO resulted in a dose-dependent inhibition of basal and acetylcholine-stimulated NO production and eNOS protein expression and also led to a significant dose-dependent stimulation of DNA synthesis in endothelial cells. Acetylcholine 57-70 nitric oxide synthase 3 Homo sapiens 100-104