Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8269238 | Free Radical Biology and Medicine | 2015 | 14 Pages |
Abstract
Proposed mechanisms for COX-2- and ROS-induced renal endothelial dysfunction in obesity. See Discussion for details. AA, arachidonic acid; ACh, acetylcholine, COX-1, cyclooxygenase 1; COX-2, cyclooxygenase 2; EC, endothelial cell; eNOS, endothelial nitric oxide synthase; IP, Prostacyclin receptor; NO, nitric oxide; PGI2, prostacyclin; TXA2, thromboxane A2; TP, TXA2/PGH2 receptor; VSMC, vascular smooth muscle cell. Inhibition of contraction240
Keywords
TXA2/PGH2 receptorET-1HFDNOSPHECOX-2TxA2PSSKPSSVSMCOXROSHydrogen peroxidecyclooxygenaseAChEndothelial dysfunctionAcetylcholineendothelin-1Thromboxane A2Oxidative stressphysiological saline solutionHigh fat dietrenal arteriesVascular smooth musclephenylephrineObesityInsulin resistanceObese Zucker ratNitric oxidenitric oxide synthaseH2O2prostacyclinProstaglandin F2αReactive oxygen speciesProstacyclin receptor
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Authors
Mercedes Muñoz, Ana Sánchez, MarÃa Pilar MartÃnez, Sara Benedito, Maria-Elvira López-Oliva, Albino GarcÃa-Sacristán, Medardo Hernández, Dolores Prieto,