PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22886025-3 2013 cGMP levels were significantly increased while AbetaPP and BACE1 protein levels were statistically lower in cerebral microvessels from nitroglycerin-treated eNOS-/- mice as compared to vehicle-treated mice. Nitroglycerin 135-148 nitric oxide synthase 3, endothelial cell Mus musculus 157-161 25158065-2 2014 Previously, we have shown that the vasodilatory action of GTN is dependent on endothelial nitric oxide synthase (eNOS/NOS3) activity. Nitroglycerin 58-61 nitric oxide synthase 3, endothelial cell Mus musculus 78-111 25158065-2 2014 Previously, we have shown that the vasodilatory action of GTN is dependent on endothelial nitric oxide synthase (eNOS/NOS3) activity. Nitroglycerin 58-61 nitric oxide synthase 3, endothelial cell Mus musculus 118-122 25158065-5 2014 Therefore, we hypothesized that nitrate tolerance induced by persistent GTN treatment results from NOS3 dysfunction and vascular toxicity. Nitroglycerin 72-75 nitric oxide synthase 3, endothelial cell Mus musculus 99-103 25158065-6 2014 Exposure to GTN for 48-72 h resulted in nitrosation and depletion (>50%) of Cav-1, NOS3 uncoupling as measured by an increase in peroxynitrite production (>100%), and endothelial toxicity in cultured cells. Nitroglycerin 12-15 nitric oxide synthase 3, endothelial cell Mus musculus 86-90 25158065-7 2014 In the Cav-1 deficient mice, NOS3 dysfunction was accompanied by GTN tolerance (>50% dilation inhibition at low GTN concentrations). Nitroglycerin 115-118 nitric oxide synthase 3, endothelial cell Mus musculus 29-33 25158065-8 2014 In conclusion, GTN tolerance results from Cav-1 modification and depletion by GTN that causes persistent NOS3 activation and uncoupling, preventing it from participating in GTN-medicated vasodilation. Nitroglycerin 15-18 nitric oxide synthase 3, endothelial cell Mus musculus 105-109 25158065-8 2014 In conclusion, GTN tolerance results from Cav-1 modification and depletion by GTN that causes persistent NOS3 activation and uncoupling, preventing it from participating in GTN-medicated vasodilation. Nitroglycerin 78-81 nitric oxide synthase 3, endothelial cell Mus musculus 105-109 25158065-8 2014 In conclusion, GTN tolerance results from Cav-1 modification and depletion by GTN that causes persistent NOS3 activation and uncoupling, preventing it from participating in GTN-medicated vasodilation. Nitroglycerin 78-81 nitric oxide synthase 3, endothelial cell Mus musculus 105-109 12969888-10 2004 Left ventricular end-diastolic pressure was significantly (P < 0.05 vs. NTG) reduced in the eNOS TG-Kobe strain at 7 days of reperfusion. Nitroglycerin 75-78 nitric oxide synthase 3, endothelial cell Mus musculus 95-99 12527144-3 2003 In the female eNOS (+/+) mice, but not in males, in vitro NTG (0.73 mM) induced significant increases in the release of CGRP-like immunoreactivity (CGRP-LI) from the aorta and the heart but not from the small intestine. Nitroglycerin 58-61 nitric oxide synthase 3, endothelial cell Mus musculus 14-18 12527144-5 2003 These results suggest that NTG-induced CGRP release is eNOS-dependent and tissue- and gender-selective. Nitroglycerin 27-30 nitric oxide synthase 3, endothelial cell Mus musculus 55-59