Effects of Angiotensin II Infusion on the Expression and Function of NAD(P)H Oxidase and Components of Nitric Oxide/cGMP Signaling

By H. Mollnau, M. Wendt, K. Szöcs, B. Lassègue, Eberhard Schulz, M. Oelze, Huige Li, Martin Bodenschatz, Michael August, A. Kleschyov and 6 more. Circulation Research, 2002

707 citations recorded by the source corpus.

Subfields: Biochemistry, Cardiology and Cardiovascular Medicine, Physiology

View Paper: https://www.semanticscholar.org/paper/9afd0eaf8cdcf9fbf05c81182ecb856d6116ac14

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Biochemistry

1. U. Förstermann
2. S. Reddy
3. Khiem A. Tran
4. Asrar B. Malik
5. A. Shah
6. M. Siddiqui
7. Jian-Mei Li
8. M. Mittal

In Cardiology and Cardiovascular Medicine

1. U. Förstermann
2. A. Shah

In Physiology

1. U. Förstermann
2. R. Clempus
3. A. Shah
4. B. Lassègue
5. S. Reddy
6. Khiem A. Tran
7. Asrar B. Malik
8. M. Siddiqui

Citations in the corpus

• Vascular NAD(P)H oxidases: specific features, expression, and regulation. (2003, methodology): “Conversely, a concomitant decrease in blood pressure, vascular oxidase activity, and expression of p22phox mRNA was observed by treatment of ANG II-infused rats with the PKC inhibitor chelerythrine (133) or with an AT1 receptor antagonist (54, 234).”
• Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology. (2004, background): “Endothelial NADPH oxidase activity is increased by 1) mechanical forces such as oscillatory shear stress (67); 2) hypoxia-reoxygenation (77, 136, 141), flow cessation (111), membrane depolarization (4, 140), nutrient deprivation (106), or ischemia (4, 111); 3) G protein-coupled receptor agonists suc”
• Nitric oxide synthases: regulation and function. (2012, background): “In experimental diabetes mellitus and angiotensin II-induced hypertension, this has been shown to be mediated by protein kinase C (PKC).(168,169) Expression of endothelial NOS is also increased in vascular disease.”
• NADPH Oxidases in Cardiovascular Health and Disease (2006, positive): “oxidase activity is increased in rats made hypertensive by chronic Ang II infusion (283), together with increases in the expression of Nox1, 2, and 4 (246) and p22phox mRNA (96).”
• Cardiovascular disease burden from ambient air pollution in Europe reassessed using novel hazard ratio functions (2019, background): “Fine particulate matter has been shown to cause vascular (endothelial) dysfunction by activating molecular pathways leading to increased oxidative stress(11) through mechanisms that are strikingly similar to those underlying vascular dysfunction established in the setting of diabetes(28) and hyperte”
• Reactive Oxygen Species in Inflammation and Tissue Injury (2014, positive): “The superoxide generated by eNOS uncoupling has been implicated in a variety of inflammatory conditions, including acute lung injury (385), diabetes mellitus (178), and Ang II-induced hypertension (298).”