Angiotensin II, NADPH oxidase, and redox signaling in the vasculature.
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There is still a paucity of information on how Ang II exerts cell-specific effects through ROS and how Nox isoforms are differentially regulated by Ang II, and exact mechanisms whereby ROS induce oxidative modifications of signaling molecules mediating Ang II actions remain elusive.Abstract:
Significance: Angiotensin II (Ang II) influences the function of many cell types and regulates many organ systems, in large part through redox-sensitive processes. In the vascular system, Ang II is a potent vasoconstrictor and also promotes inflammation, hypertrophy, and fibrosis, which are important in vascular damage and remodeling in cardiovascular diseases. The diverse actions of Ang II are mediated via Ang II type 1 and Ang II type 2 receptors, which couple to various signaling molecules, including NADPH oxidase (Nox), which generates reactive oxygen species (ROS). ROS are now recognized as signaling molecules, critically placed in pathways activated by Ang II. Mechanisms linking Nox and Ang II are complex and not fully understood. Recent Advances: Ang II regulates vascular cell production of ROS through various recently characterized Noxs, including Nox1, Nox2, Nox4, and Nox5. Activation of these Noxs leads to ROS generation, which in turn influences many downstream signaling targets of Ang II, including MAP kinases, RhoA/Rho kinase, transcription factors, protein tyrosine phosphatases, and tyrosine kinases. Activation of these redox-sensitive pathways regulates vascular cell growth, inflammation, contraction, and senescence. Critical Issues: Although there is much evidence indicating a role for Nox/ROS in Ang II function, there is still a paucity of information on how Ang II exerts cell-specific effects through ROS and how Nox isoforms are differentially regulated by Ang II. Moreover, exact mechanisms whereby ROS induce oxidative modifications of signaling molecules mediating Ang II actions remain elusive. Future Directions: Future research should elucidate these issues to better understand the significance of Ang II and ROS in vascular (patho) biology. Antioxid. Redox Signal. 19, 1110–1120.read more
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References
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Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells.
TL;DR: The ability of Ang II to stimulate superoxide anion formation is examined and the identity of the oxidases responsible for its production is investigated to suggest that Ang II specifically activates enzyme systems that promote superoxide generation and raise the possibility that these pathways function as second messengers for long-term responses, such as hypertrophy or hyperplasia.
Journal ArticleDOI
Angiotensin II-mediated hypertension in the rat increases vascular superoxide production via membrane NADH/NADPH oxidase activation. Contribution to alterations of vasomotor tone.
Sanjay Rajagopalan,S Kurz,Thomas Münzel,Margaret M. Tarpey,Bruce A. Freeman,Kathy K. Griendling,David G. Harrison +6 more
TL;DR: Forms of hypertension associated with elevated circulating levels of angiotensin II may have unique vascular effects not shared by other forms of hypertension because they increase vascular smooth muscle .O2- production via NADH/NADPH oxidase activation.
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Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system
TL;DR: This review focuses on the structure and function of AT(1) receptors and the major signaling mechanisms by which angiotensin influences cardiovascular physiology and pathology.
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Superoxide anion radical (O2-.), superoxide dismutases, and related matters.
TL;DR: This review will describe only aspects of the biology of oxygen radicals that currently engage the interest of the writer and Hopefully they will also be of interest to the reader.
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Vascular NAD(P)H oxidases: specific features, expression, and regulation
Bernard Lassègue,Roza E. Clempus +1 more
TL;DR: Members of this enzyme family appear to be important in vascular biology and disease and constitute promising targets for future therapeutic interventions.
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