Angiotensin II, NADPH oxidase, and redox signaling in the vasculature.
Reads0
Chats0
TLDR
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
Citations
More filters
Journal ArticleDOI
Chronic iron overload in rats increases vascular reactivity by increasing oxidative stress and reducing nitric oxide bioavailability.
Vinicius Bermond Marques,Tatiani Botelho Nascimento,Rogério Faustino Ribeiro,Gilson Brás Broseghini-Filho,Emilly M. Rossi,Jones Bernades Graceli,Leonardo dos Santos +6 more
TL;DR: It is demonstrated that chronic iron overload is associated with altered vascular reactivity and the loss of endothelial modulation of the vascular tone and reduced nitric oxide bioavailability and may be a result of increased production of reactive oxygen species and local renin-angiotensin system activation.
Journal ArticleDOI
Exendin-4 alleviates angiotensin II-induced senescence in vascular smooth muscle cells by inhibiting Rac1 activation via a cAMP/PKA-dependent pathway
TL;DR: Exendin-4 confers resistance to ANG II-induced superoxide anion generation from NAD(P)H oxidase and the resultant VSMC senescence by inhibiting Rac1 activation via a cAMP/PKA-dependent pathway.
Journal ArticleDOI
ACE2/Ang-(1–7)/Mas axis stimulates vascular repair-relevant functions of CD34+ cells
Neha Singh,Shrinidh Joshi,Lirong Guo,Matthew B. Baker,Yan Li,Ronald K. Castellano,Mohan K. Raizada,Yagna P. R. Jarajapu +7 more
TL;DR: It is suggested that ACE2/Ang-(1-7)/Mas pathway stimulates functions of CD34(+) cells that are cardiovascular protective, whereas Ang II attenuates these functions by acting on MNCs.
Journal ArticleDOI
Bang-Bang Model for Regulation of Local Blood Flow
TL;DR: A model of regulation in which muscle contraction and active hyperemia are considered the physiologically normal state is proposed, which provides a clear and unambiguous interpretation of the mechanism to balance tissue demand with a sufficient supply of nutrients and oxygen.
Journal ArticleDOI
Hemoglobin-associated oxidative stress in the pericardial compartment of postoperative cardiac surgery patients
Philip A. Kramer,Balu K. Chacko,Saranya Ravi,Michelle S. Johnson,Tanecia Mitchell,Stephen Barnes,Alireza Arabshahi,Louis J. Dell'Italia,David J. George,Chad Steele,James F. George,Victor M. Darley-Usmar,Spencer J. Melby +12 more
TL;DR: It is concluded that PO-PCF is highly pro-oxidant and speculate that it may contribute to the risk of postoperative complications and that the potential interaction between inflammatory cell-derived hydrogen peroxide with hemoglobin is associated with oxidative stress.
References
More filters
Journal ArticleDOI
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.
Journal ArticleDOI
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.
Journal ArticleDOI
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.
Journal ArticleDOI
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.
Related Papers (5)
The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology
Karen Bedard,Karl-Heinz Krause +1 more