Abstract
This chapter considers systems controlling the origins and mechanisms through which nitric oxide (NO) and reactive oxygen species (ROS) regulate vascular function. Oxidases in various cell types within and surrounding the vasculature such as endothelium, vascular smooth muscle, and inflammatory cells are sources of NO and ROS that regulate vascular function through many processes controlling the activities of specific NO synthase (NOS) and oxidase enzymes. Each NO and ROS has specific chemical properties and interactions with enzymes and/or cofactors. Many of these interactions enable them to control signaling processes regulating the function of cells in the vasculature ranging from physiological mechanisms such as oxygen sensing, to many pathophysiological processes (increased pressure, shear, vascular disease-associated vasoconstrictors) altering the regulation of vascular function.
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsAbbreviations
- ecSOD:
-
Extracellular superoxide dismutase (SOD3)
- eNOS:
-
Endothelial nitric oxide synthase (NOS3)
- ETC:
-
Electron transport chain
- H2O2 :
-
Hydrogen peroxide
- HPV:
-
Hypoxic pulmonary vasoconstriction
- NADH:
-
Nicotinamide adenine dinucleotide (reduced)
- NADPH:
-
Nicotinamide adenine dinucleotide phosphate (reduced)
- NAD(P)H:
-
NADH and NADPH
- NO:
-
Nitric oxide
- iNOS:
-
Inducible or inflammatory nitric oxide synthase (NOS2)
- nNOS:
-
Neuronal nitric oxide synthase (NOS1)
- NOS:
-
Nitric oxide synthase
- Nox:
-
NADPH oxidase
- Nrf2:
-
Nuclear factor (erythroid-derived 2)-like 2
- O2 – :
-
Superoxide anion
- PG:
-
Prostaglandin
- PKG:
-
Protein kinase G
- RNS:
-
Reactive nitric oxide-derived species
- ROS:
-
Reactive oxygen species
- SOD:
-
Superoxide dismutase
References
Abraham NG, Kappas A (2008) Pharmacological and clinical aspects of heme oxygenase. Pharmacol Rev 60:79–127
Addabbo F, Montagnani M, Goligorsky MS (2009) Mitochondria and reactive oxygen species. Hypertension 53:885–892
Ata H, Rawat DK, Lincoln T, Gupte SA (2011) Mechanism of glucose-6-phosphate dehydrogenase-mediated regulation of coronary artery contractility. Am J Physiol Heart Circ Physiol 300:H2054–H2063
Boueiz A, Damarla M, Hassoun PM (2008) Xanthine oxidoreductase in respiratory and cardiovascular disorders. Am J Physiol Lung Cell Mol Physiol 294:L830–L840
Dai D-F, Rabinovitch PS, Ungvari Z (2012) Mitochondria and cardiovascular aging. Circ Res 110:1109–1124
Dikalova AE, Góngora MC, Harrison DG, Lambeth JD, Dikalov S, Griendling KK (2010) Upregulation of Nox1 in vascular smooth muscle leads to impaired endothelium-dependent relaxation via eNOS uncoupling. Am J Physiol Heart Circ Physiol 299:H673–H679
Duncker DJ, Bache RJ (2008) Regulation of coronary blood flow during exercise. Physiol Rev 88:1009–1086
Forman HJ, Fukuto JM, Torres M (2004) Redox signaling: thiol chemistry defines which reactive oxygen and nitrogen species can act as second messengers. Am J Physiol Cell Physiol 287:246–256
Gupte SA, Kaminski PM, George S, Kouznestova L, Olson SC, Matthew R, Hintze TH, Wolin MS (2009) Peroxide generation by p47phox-Src activation of Nox2 has a key role in protein kinase C-induced arterial smooth muscle contraction. Am J Physiol Heart Circ Physiol 296:H1048–H1057
Gupte RS, Rawat DK, Chettimada S, Cioffi DL, Wolin MS, Gerthoffer WT, McMurtry IF, Gupte SA (2010) Activation of glucose-6-phosphate dehydrogenase promotes acute hypoxic pulmonary artery contraction. J Biol Chem 285:19561–19571
Ignarro LJ, Byrns RE, Buga GM, Wood KS, Chaudhuri G (1988) Pharmacological evidence that endothelium-derived relaxing factor is nitric oxide: use of pyrogallol and superoxide dismutase to study endothelium-dependent and nitric oxide-elicited vascular smooth muscle relaxation. J Pharmacol Exp Ther 244:181–189
Kukreja RC, Kontos HA, Hess ML, Ellis EF (1986) PGH synthase and lipoxygenase generate superoxide in the presence of NADH or NADPH. Circ Res 59:612–619
Lassègue B, San Martín A, Griendling KK (2012) Biochemistry, physiology, and pathophysiology of NADPH oxidases in the cardiovascular system. Circ Res 110:1364–1390
Li A-M, Shah AM (2004) Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology. Am J Physiol Regul Integr Comp Physiol 287:R1014–R1030
Lincoln TM, Dey N, Sellak H (2001) Invited review: cGMP-dependent protein kinase signaling mechanisms in smooth muscle: from the regulation of tone to gene expression. J Appl Physiol 91:1421–1430
Luiking YC, Ten Have GAM, Wolfe RR, Deutz NEP (2012) Arginine de novo and nitric oxide production in disease states. Am J Physiol Endocrinol Metab 303:E1177–E1189
Moncada S, Palmer RM, Higgs EA (1991) Nitric oxide: physiology, pathophysiology, and pharmacology. Pharmacol Rev 43:109–142
Moudgil R, Michelakis ED, Archer SL (2005) Hypoxic pulmonary vasoconstriction. J Appl Physiol 98:390–403
Neo BH, Kandhi S, Ahmad M, Wolin MS (2010) Redox regulation of guanylate cyclase and protein kinase G in vascular responses to hypoxia. Respir Physiol Neurobiol 174:259–264
Palmer RM, Ferrige AG, Moncada S (1987) Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor. Nature 327(6122):524–526
Pacher P, Beckman JS, Liaudet L (2007) Nitric oxide and peroxynitrite in health and disease. Physiol Rev 87:315–424
Pryor WA, Houk KN, Foote CS, Fukuto JM, Ignarro LJ, Squadrito GL, Davies KJA (2006) Free radical biology and medicine: it’s a gas, man! Am J Physiol Regul Integr Comp Physiol 291:R491–R511
Stasch J-P, Schmidt PM, Nedvetsky PI, Nedvetskaya TY, Arun Kumar HSA, Meurer S, Deile M, Taye A, Knorr A, Lapp H, Müller H, Turgay Y, Rothkegel C, Tersteegen A, Kemp-Harper B, Müller-Esterl W, Schmidt HHHW (2006) Targeting the heme-oxidized nitric oxide receptor for selective vasodilatation of diseased blood vessels. J Clin Invest 116:2552–2561
Ungvari Z, Wolin MS, Csiszar A (2006) Mechanosensitive production of reactive oxygen species in endothelial and smooth muscle cells: role in microvascular remodeling? Antioxid Redox Signal 8:1121–1129
Waypa GB, Schumacker PT (2005) Hypoxic pulmonary vasoconstriction: redox events in oxygen sensing. J Appl Physiol 98:404–414
Waypa GB, Marks JD, Guzy R, Mungai PT, Schriewer J, Dokic D, Schumacker PT (2010) Hypoxia triggers subcellular compartmental redox signaling in vascular smooth muscle cells. Circ Res 106:526–535
Wolin MS (2000) Interactions of oxidants with vascular signaling systems. Arterioscler Thromb Vasc Biol 20:1430–1442
Wolin MS, Ahmad M, Gupte SA (2005) Oxidant and redox signaling in vascular oxygen sensing mechanisms: basic concepts, current controversies, and potential importance of cytosolic NADPH. Am J Physiol Lung Cell Mol Physiol 289:L159–L173
Zhang G, Zhang F, Muh R, Yi F, Chalupsky K, Cai H, Li PL (2007) Autocrine/paracrine pattern of superoxide production through NAD(P)H oxidase in coronary arterial myocytes. Am J Physiol Heart Circ Physiol 292:H483–H495
Acknowledgments
Recent studies from the authors’ laboratory have been funded by USPHS grants HL031069, HL043023, HL066331, and HL115124.
Author information
Authors and Affiliations
Corresponding author
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2014 Springer Science+Business Media, LLC
About this chapter
Cite this chapter
Wolin, M.S. (2014). Reactive Oxygen Species and Nitric Oxide in Vascular Function. In: Tsukahara, H., Kaneko, K. (eds) Studies on Pediatric Disorders. Oxidative Stress in Applied Basic Research and Clinical Practice. Springer, New York, NY. https://doi.org/10.1007/978-1-4939-0679-6_2
Download citation
DOI: https://doi.org/10.1007/978-1-4939-0679-6_2
Published:
Publisher Name: Springer, New York, NY
Print ISBN: 978-1-4939-0678-9
Online ISBN: 978-1-4939-0679-6
eBook Packages: Biomedical and Life SciencesBiomedical and Life Sciences (R0)