Table 1. Modulative effects of AGEs on vascular responses mediated by vasoactive substances.
| AGEs | Animal/tissue | Molecular target | Impact on vascular function | References |
| AGE-BSA | Rat/aorta | ↓ NO bioavailability ↑ Arginase ↑ NADPH oxidase |
↓ ACh-induced relaxation | El-Bassossy et al., 2018 (31) |
| AGE-BSA | Rat/aorta | ↓ NO bioavailability ↓ DDAH |
↓ ACh-induced relaxation | Yin and Xiong, 2005 (40) |
| MGO | Rat/superior mesenteric artery | ↓ NO bioavailability ↓ eNOS ↑ NADPH oxidase |
↓ ACh-induced relaxation | Mukohda et al., 2013 (91) |
| MGO | Rat/aorta | ↓ NO bioavailability ↓ eNOS phosphorylation (Ser1177) ↓ AMPKα phosphorylation (Thr172) |
↓ ACh-induced relaxation | Turkseven et al., 2014 (92) |
| AGE-BSA | Rat/mesenteric arteries | ↓ SKCa, IKCa | ↓ EDHF-mediated relaxation | Zhao et al., 2014 (93) |
| CML | Rat/perfused coronary arteries | ↑ ACh-induced contraction | Kamata et al., 2009 (94) | |
| MGO | Rat/superior mesenteric artery, aorta | ↑ BKCa | ↓ NAd-induced contraction | Mukohda et al., 2009 (66) |
| MGO | Rat superior mesenteric artery | ↑ Superoxide (by NADPH oxidase) | ↓ NAd-induced contraction | Mukohda et al., 2012 (67) |
| AGE-BSA | Rat/carotid artery | ↑ H2O2, BKCa, OCT3 | ↓ NAd-induced contraction | Matsumoto et al., 2020 (68) |
| MGO | Rat/carotid artery | ↑ ROS (endothelium derived) | ↑ Ang II-induced contraction | Mukohda et al., 2010 (74) |
| MGO | Rat/aortaRat/perfused kidney | ↑ Voltage-activated Ca2+ influx ↑ NOX ↑ PKC |
↑ PE-, Ang II-, vasopressin-, and KCl-induced contractions | Eid et al., 2018 (95) |
| CML | Rat/perfused coronary arteries | ↑ big ET-1- and ET-1-induced contractions | Matsumoto et al., 2010 (84) | |
| AGE-BSA | Rat/carotid artery | ↑ COX/TxS/TP receptor | ↑ UDP-induced contraction | Matsumoto et al., 2019 (86) |
| MGO | Rat/carotid artery | ↑ p38 MAPK, PKC, oxidative stress | ↑ UDP-induced contraction | Matsumoto et al., 2021 (87) |
ACh: acetylcholine; AGEs: advanced glycation end products; AGE-BSA: advanced glycation end products-bovine serum albumin; AMPK: AMP-activated protein kinase; Ang II: angiotensin II; Ca2+: calcium; CML: Nε-carboxymethyl-lysine; COX: cyclooxygenase; DDAH: dimethylarginine dimethylaminohydrolase; EDHF: endothelium-derived hyperpolarizing factor; eNOS: endothelial nitric oxide synthase; IKCa: intermediate-conductance calcium-activated potassium channels; MAPK: mitogen-activated protein kinase; MGO: methylglyoxal; NAd: noradrenaline; NO: nitric oxide; NOX: NADPH oxidase; OCT3: organic cation transporter 3; PE: phenylephrine; PKC: protein kinase C; ROS: reactive oxygen species; SKCa: small-conductance calcium-activated potassium channels; TP: thromboxane-prostanoid; TxS: thromboxane synthase; UDP: uridine diphosphate.