PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 17117376-2 2007 Using angiotensin II as the model system, we demonstrate that nitrite catalyzed the selective iodination of the peptide at the N-terminus in an acidic solution. Nitrites 62-69 angiotensinogen Homo sapiens 6-20 25312440-3 2015 We investigated the hypothesis that inorganic nitrate and nitrite attenuate reactivity of renal microcirculation and blood pressure responses to angiotensin II (ANG II) by modulating nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and NO bioavailability. Nitrites 58-65 angiotensinogen Homo sapiens 145-159 25312440-3 2015 We investigated the hypothesis that inorganic nitrate and nitrite attenuate reactivity of renal microcirculation and blood pressure responses to angiotensin II (ANG II) by modulating nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and NO bioavailability. Nitrites 58-65 angiotensinogen Homo sapiens 161-167 25312440-5 2015 Contractions to ANG II (34%) and simultaneous NO synthase inhibition (56%) were attenuated by nitrite (18% and 26%). Nitrites 94-101 angiotensinogen Homo sapiens 16-22 25312440-6 2015 In a model of oxidative stress (superoxide dismutase-1 knockouts), abnormal ANG II-mediated arteriolar contractions (90%) were normalized by nitrite (44%). Nitrites 141-148 angiotensinogen Homo sapiens 76-82 25312440-10 2015 In preglomerular vascular smooth muscle cells and kidney cortex, nitrite reduced both basal and ANG II-induced NADPH oxidase activity. Nitrites 65-72 angiotensinogen Homo sapiens 96-102 11001767-5 2000 Angiotensin II (ANG II, 100 nM) increased EC production of nitrate/nitrite by 2.4-fold. Nitrites 67-74 angiotensinogen Homo sapiens 0-14 11001767-5 2000 Angiotensin II (ANG II, 100 nM) increased EC production of nitrate/nitrite by 2.4-fold. Nitrites 67-74 angiotensinogen Homo sapiens 16-22 33126056-0 2021 Oral nitrite treatment increases S-nitrosylation of vascular protein kinase C and attenuates the responses to angiotensin II. Nitrites 5-12 angiotensinogen Homo sapiens 110-124 10642319-4 2000 Nitrate/nitrite production in AdeNOS-transduced ZG cells increased from 0.15+/-0.01 to 0.27+/-0.01 micromol/L after stimulation with 1 nmol/L angiotensin II. Nitrites 8-15 angiotensinogen Homo sapiens 142-156 10642319-5 2000 The treatment of AdeNOS-transduced cells with 30 micromol/L L-nitro-arginine decreased angiotensin II-stimulated nitrite production from 0.27+/-0. Nitrites 113-120 angiotensinogen Homo sapiens 87-101 10642319-7 2000 Basal and angiotensin II-stimulated nitrite production was not increased in AdbetaGal-transduced or control cells. Nitrites 36-43 angiotensinogen Homo sapiens 10-24 33126056-4 2021 Our results show that oral nitrite treatment enhances circulating RXNO concentrations (measured by ozone-based chemiluminescence methods), increases aortic protein kinase C (PKC) nitrosylation (measured by resin-assisted capture SNO-RAC method), and reduces both angiotensin II-induced vasoconstriction (isolated aortic ring preparation) and hypertensive (in vivo invasive blood pressure measurements) effects implicating PKC nitrosylation as a key mechanism for the responses to oral nitrite. Nitrites 27-34 angiotensinogen Homo sapiens 263-277 33126056-9 2021 Together, these results are consistent with the idea that PKC nitrosylation in the vasculature may underlie oral nitrite treatment-induced reduction in the vascular and hypertensive responses to angiotensin II. Nitrites 113-120 angiotensinogen Homo sapiens 195-209 24178685-8 1996 Ang II also inhibited the IL-1beta induced nitrite accumulation by SMCs. Nitrites 43-50 angiotensinogen Homo sapiens 0-6 7512570-2 1994 A potent vasoconstrictor, angiotensin II (Ang II), which causes a rapid phospholipase C-mediated phosphoinositide hydrolysis via the Ang II type 1 (AT1) receptor in VSMC, by itself did not stimulate the production of nitrite, a stable metabolite of NO, but dose dependently inhibited the IL-1 beta-induced nitrite production. Nitrites 217-224 angiotensinogen Homo sapiens 26-40 7512570-2 1994 A potent vasoconstrictor, angiotensin II (Ang II), which causes a rapid phospholipase C-mediated phosphoinositide hydrolysis via the Ang II type 1 (AT1) receptor in VSMC, by itself did not stimulate the production of nitrite, a stable metabolite of NO, but dose dependently inhibited the IL-1 beta-induced nitrite production. Nitrites 217-224 angiotensinogen Homo sapiens 42-48 7512570-2 1994 A potent vasoconstrictor, angiotensin II (Ang II), which causes a rapid phospholipase C-mediated phosphoinositide hydrolysis via the Ang II type 1 (AT1) receptor in VSMC, by itself did not stimulate the production of nitrite, a stable metabolite of NO, but dose dependently inhibited the IL-1 beta-induced nitrite production. Nitrites 217-224 angiotensinogen Homo sapiens 133-139 7512570-2 1994 A potent vasoconstrictor, angiotensin II (Ang II), which causes a rapid phospholipase C-mediated phosphoinositide hydrolysis via the Ang II type 1 (AT1) receptor in VSMC, by itself did not stimulate the production of nitrite, a stable metabolite of NO, but dose dependently inhibited the IL-1 beta-induced nitrite production. Nitrites 306-313 angiotensinogen Homo sapiens 26-40 7512570-2 1994 A potent vasoconstrictor, angiotensin II (Ang II), which causes a rapid phospholipase C-mediated phosphoinositide hydrolysis via the Ang II type 1 (AT1) receptor in VSMC, by itself did not stimulate the production of nitrite, a stable metabolite of NO, but dose dependently inhibited the IL-1 beta-induced nitrite production. Nitrites 306-313 angiotensinogen Homo sapiens 42-48 7512570-2 1994 A potent vasoconstrictor, angiotensin II (Ang II), which causes a rapid phospholipase C-mediated phosphoinositide hydrolysis via the Ang II type 1 (AT1) receptor in VSMC, by itself did not stimulate the production of nitrite, a stable metabolite of NO, but dose dependently inhibited the IL-1 beta-induced nitrite production. Nitrites 306-313 angiotensinogen Homo sapiens 133-139 7512570-6 1994 Ang II also inhibited increases in nitrite production and iNOS mRNA and protein levels caused by tumor necrosis factor alpha. Nitrites 35-42 angiotensinogen Homo sapiens 0-6 7534178-3 1994 AII by itself did not stimulate the production of nitrite, a stable metabolite of NO, but dose-dependently inhibited IL1 beta-induced nitrite production. Nitrites 134-141 angiotensinogen Homo sapiens 0-3 7534178-5 1994 In parallel with the decrease in nitrite production, AII suppressed IL1 beta-induced increases in iNOS mRNA and protein levels, as measured by Northern blotting using an iNOS cDNA probe and by immunoblotting using an anti-iNOS antibody, respectively. Nitrites 33-40 angiotensinogen Homo sapiens 53-56 7534178-6 1994 AII also inhibited the increases in nitrite production and iNOS mRNA and protein levels caused by TNF alpha. Nitrites 36-43 angiotensinogen Homo sapiens 0-3 32141427-5 2020 Using a loss-of-function assay and inhibitor treatment, we found that AGT knockdown inhibited the increase of IL-1beta, matrix metalloproteinase (MMP)-13 and nitrite in IL-6-induced chondrocytes through blocking the renin-angiotensin system (RAS). Nitrites 158-165 angiotensinogen Homo sapiens 70-73