Nitric Oxide Signalling In Cardiovascular Health And Disease Pdf
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- Nitric Oxide Signalling in Vascular Control and Cardiovascular Risk
- Nitric oxide signalling in cardiovascular health and disease
- Nitric Oxide: A Regulator of Cellular Function in Health and Disease
- Biological functions of nitric oxide
The initial identification of NO as an endothelium-derived relaxing factor EDRF [ 3 ] generated great interest in its function in vascular biology. Over the following years, however, the focus on NO research rapidly expanded from the vascular system to its role in immunity and inflammation, the nervous system, pregnancy, aging, and cell death.
Victor W. Liu, Paul L. Nitric oxide NO is a gaseous molecule that plays many key roles in the cardiovascular system. Each of the enzymes that generate NO—neuronal, inducible and endothelial NO synthase—has been genetically disrupted in mice. This review discusses the cardiovascular phenotypes of each of the NO synthase NOS gene knockout mice, and the insights gained into the roles of NO in the cardiovascular system.
Nitric Oxide Signalling in Vascular Control and Cardiovascular Risk
Nitric oxide nitrogen monoxide is a molecule and chemical compound with chemical formula of N O. In mammals including humans, nitric oxide is a signaling molecule involved in many physiological and pathological processes. Standard pharmaceuticals such as nitroglycerine and amyl nitrite are precursors to nitric oxide. Low levels of nitric oxide production are typically due to ischemic damage in the liver. As a consequence of its importance in neuroscience , physiology , and immunology , nitric oxide was proclaimed " Molecule of the Year " in Platelet -derived factors, shear stress , acetylcholine , and cytokines stimulate the production of NO by endothelial nitric oxide synthase eNOS. NO production by eNOS is dependent on calcium - calmodulin and other cofactors.
Nitric Oxide NO is an essential signaling molecule with diverse physiological functions in humans. The steady-state concentration and site of production of nitric oxide determine its effects in biological systems. The human cells are exposed to both beneficial and harmful effects of NO. These dual effects of NO could depend on its local concentration in the cells. Additionally, the rate of synthesis, translocation, direct interaction with other molecules, and signals contribute to the biochemical and physiological effects of NO. In this review, the biochemical and physiological role of NO, particularly in health and disease as touching on cell signaling, oxidative stress, immunity, as well as cardiovascular protection amongst others, is focused on.
Nitric oxide signalling in cardiovascular health and disease
This is an open access article distributed under the terms of Creative Commons Attribution License. Microorganisms and toxic factors are the predominant causative agents of periodontitis. In response to activated tissues, macrophages and lymphocytes produce matrix metalloproteinases and inflammatory factors, such as interleukin-1 IL-1 and tumor necrosis factor TNF 1 , which serve essential roles in periodontal tissue destruction. Therefore, many inflammatory mediators are considered to be crucial in the development of early periodontal disease with nitric oxide NO the main inflammatory factor in this disease 2. NO is an extremely unstable, fat-soluble gas at room temperature that can diffuse rapidly through biofilms.
Nitric oxide (NO) signalling has pleiotropic roles in biology and a crucial function in cardiovascular homeostasis. In this Review, Balligand and.
Nitric Oxide: A Regulator of Cellular Function in Health and Disease
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Cardiovascular Risk Factors.
Biological functions of nitric oxide
Regulation of endothelial derived nitric oxide in health and disease. Endothelial nitric oxide synthase eNOS is the primary physiological source of nitric oxide NO that regulates cardiovascular homeostasis. Historically eNOS has been thought to be a constitutively expressed enzyme regulated by calcium and calmodulin. However, in the last five years it is clear that eNOS activity and NO release can be regulated by post-translational control mechanisms fatty acid modification and phosphorylation and protein-protein interactions with caveolin-1 and heat shock protein 90 that direct impinge upon the duration and magnitude of NO release. This review will summarize this information and apply the post-translational control mechanisms to disease states. Key words: nitric oxide - endothelium - caveolin-1 - heat shock protein 90 - atherosclerosis - inflammation. In the past decade the importance of the vascular endothelium as a multifunctional regulator of vascular smooth muscle physiology and pathophysiology has been appreciated.
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