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Nitric oxide in the cardiovascular system: a simple molecule with complex actions.

Strijdom H, Chamane N, Lochner A - Cardiovasc J Afr (2009 Sep-Oct)

Bottom Line: However, due to various complex underlying cellular mechanisms, the actions of NO often seem to be contradictory.NO is a promising candidate molecule that could find therapeutic application.For this to be achieved, a sound understanding of this simple molecule and its complex actions is required.

View Article: PubMed Central - HTML - PubMed

Affiliation: Division of Medical Physiology, Department of Biomedical Sciences, Faculty of Health Sciences, Stellenbosch University, South Africa. jgstr@sun.ac.za

ABSTRACT
Since it was identified as the elusive endothelium-derived relaxing factor (EDRF) in the 1980s, nitric oxide (NO) has rapidly gained status as one of the most important signalling molecules in the cardiovascular system. Now, 20 years later, NO is regarded by most to be a ubiquitous mediator of cardioprotection. However, due to various complex underlying cellular mechanisms, the actions of NO often seem to be contradictory. This article sheds light on some of the mechanisms that may influence the variable actions of NO in the heart. Its role in conditions of oxygen deprivation (ischaemia and hypoxia) in particular is relevant to basic scientists and clinicians alike, since the prevalence of ischaemic heart disease is on the rise (in both the developed and the developing worlds) and novel therapeutic options are in constant demand. NO is a promising candidate molecule that could find therapeutic application. For this to be achieved, a sound understanding of this simple molecule and its complex actions is required.

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The classical NO signalling pathway. Endothelial cells lining the lumen of blood vessels express endothelial NO synthase (eNOS ), which produces physiological concentrations of NO . NO diffuses into the underlying vascular smooth muscle cells (VSMC) where the sGCcGM P-PKG pathway is activated and ultimate inhibition of the L-type calcium channel takes place, leading to VSMC relaxation and vasodilatation. sGC: soluble guanylate cyclase, GT P: guanosine triphosphate, cGM P: cyclic guanosine monophosphate, PKG: protein kinase G.
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Figure 1: The classical NO signalling pathway. Endothelial cells lining the lumen of blood vessels express endothelial NO synthase (eNOS ), which produces physiological concentrations of NO . NO diffuses into the underlying vascular smooth muscle cells (VSMC) where the sGCcGM P-PKG pathway is activated and ultimate inhibition of the L-type calcium channel takes place, leading to VSMC relaxation and vasodilatation. sGC: soluble guanylate cyclase, GT P: guanosine triphosphate, cGM P: cyclic guanosine monophosphate, PKG: protein kinase G.

Mentions: The role of NO in the maintenance of vascular homeostasis is well defined; a role that relates to the original discovery that endothelium-derived NO diffuses into underlying vascular smooth muscle cells where the classical NO-cGMP-protein kinase G (PKG) signalling pathway causes vascular relaxation (Fig. 1). Generally speaking, NO promotes a vasodilatory, anti-thrombotic and anti-inflammatory state in the vasculature; however, when the bioavailability of NO is compromised, these beneficial actions are lost and endothelial dysfunction ensues.9


Nitric oxide in the cardiovascular system: a simple molecule with complex actions.

Strijdom H, Chamane N, Lochner A - Cardiovasc J Afr (2009 Sep-Oct)

The classical NO signalling pathway. Endothelial cells lining the lumen of blood vessels express endothelial NO synthase (eNOS ), which produces physiological concentrations of NO . NO diffuses into the underlying vascular smooth muscle cells (VSMC) where the sGCcGM P-PKG pathway is activated and ultimate inhibition of the L-type calcium channel takes place, leading to VSMC relaxation and vasodilatation. sGC: soluble guanylate cyclase, GT P: guanosine triphosphate, cGM P: cyclic guanosine monophosphate, PKG: protein kinase G.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3721819&req=5

Figure 1: The classical NO signalling pathway. Endothelial cells lining the lumen of blood vessels express endothelial NO synthase (eNOS ), which produces physiological concentrations of NO . NO diffuses into the underlying vascular smooth muscle cells (VSMC) where the sGCcGM P-PKG pathway is activated and ultimate inhibition of the L-type calcium channel takes place, leading to VSMC relaxation and vasodilatation. sGC: soluble guanylate cyclase, GT P: guanosine triphosphate, cGM P: cyclic guanosine monophosphate, PKG: protein kinase G.
Mentions: The role of NO in the maintenance of vascular homeostasis is well defined; a role that relates to the original discovery that endothelium-derived NO diffuses into underlying vascular smooth muscle cells where the classical NO-cGMP-protein kinase G (PKG) signalling pathway causes vascular relaxation (Fig. 1). Generally speaking, NO promotes a vasodilatory, anti-thrombotic and anti-inflammatory state in the vasculature; however, when the bioavailability of NO is compromised, these beneficial actions are lost and endothelial dysfunction ensues.9

Bottom Line: However, due to various complex underlying cellular mechanisms, the actions of NO often seem to be contradictory.NO is a promising candidate molecule that could find therapeutic application.For this to be achieved, a sound understanding of this simple molecule and its complex actions is required.

View Article: PubMed Central - HTML - PubMed

Affiliation: Division of Medical Physiology, Department of Biomedical Sciences, Faculty of Health Sciences, Stellenbosch University, South Africa. jgstr@sun.ac.za

ABSTRACT
Since it was identified as the elusive endothelium-derived relaxing factor (EDRF) in the 1980s, nitric oxide (NO) has rapidly gained status as one of the most important signalling molecules in the cardiovascular system. Now, 20 years later, NO is regarded by most to be a ubiquitous mediator of cardioprotection. However, due to various complex underlying cellular mechanisms, the actions of NO often seem to be contradictory. This article sheds light on some of the mechanisms that may influence the variable actions of NO in the heart. Its role in conditions of oxygen deprivation (ischaemia and hypoxia) in particular is relevant to basic scientists and clinicians alike, since the prevalence of ischaemic heart disease is on the rise (in both the developed and the developing worlds) and novel therapeutic options are in constant demand. NO is a promising candidate molecule that could find therapeutic application. For this to be achieved, a sound understanding of this simple molecule and its complex actions is required.

Show MeSH
Related in: MedlinePlus