Vascular
SUPPORT
IMMUNE SUPPORT
Nitric oxide plays many important roles in the immune system. It is produced in high amounts from specialized cells of the immune system called macrophages.
DIGESTIVE SUPPORT
In the gastrointestinal tract, Nitric Oxide is involved in the regulation of regional blood flow, smooth muscle relaxation, secretory and immunological function. [1]
VASCULAR SUPPORT
Since it was identified as the elusive endothelium-derived relaxing factor in the 1980s, nitric oxide (NO) has rapidly gained status as one of the most important signalling molecules in the cardiovascular system. [1]
MOBILITY SUPPORT
Nitric oxide (NO) can modulate the release of various inflammatory mediators from a wide range of cells participating in inflammatory responses (e.g., leukocytes, macrophages, mast cells, endothelial cells, and
platelets).[1]
MEMORY SUPPORT
Nitric oxide (NO) is well established as a molecule necessary for memory processing across a wide variety of tasks and species, from odour discrimination in honey bees (Muller, 1996) to delayed recall in primates (Prendergast et al., 1997).[1]
REST SUPPORT
Nitric Oxide helps reduce anxiety and depression in part because it reduces inflammation and oxidative stress. It also restores circulation and supports healthy blood pressure, which is often elevated in people under stress and with chronic PTSD, thus becoming another risk factor for vascular dementia. [1]
Vascular Support
The groundbreaking discovery in 1987, that a previously unidentified molecule, rather loosely termed ‘endothelium-derived relaxing factor’ (EDRF), was in fact nitric oxide, caused a paradigm shift in scientists’ and clinicians’ understanding of cardiovascular physiology and pathophysiology.[2] The notion that a molecule, until then regarded as an air pollutant, could be endogenously produced and could play a role as a major cardiovascular signalling molecule, was indeed surprising, if not sensational at the time and resulted in the 1998 Nobel Prize for Medicine being awarded to the researchers involved.[1]
This discovery also culminated in an understanding of the previously unknown mechanism of action of nitroglycerine (now known to be a NOreleasing compound), a popular antiangina pectoris drug prescribed by clinicians since the early 20th century! [1]
Today NO is regarded as one of the most important mediators of biological processes in the heart and blood vessels. However, the biological effects of NO are variable, and this fact is becoming increasingly evident as our knowledge of this wonder molecule expands.[1]
The role of NO in the maintenance of vascular homeostasis is well defined; a role that relates to the original discovery that endotheliumderived NO diffuses into underlying vascular smooth muscle cells where the classical NO-cGMP-protein kinase G (PKG) signalling pathway causes vascular relaxation. Generally speaking, NO promotes a vasodilatory, antithrombotic and anti-inflammatory state in the vasculature; however, when the bioavailability of NO is compromised, these beneficial actions are lost and endothelial dysfunction ensues.[3]
Now, 20 years after discovery, nitric oxide (NO) is regarded by most to be a ubiquitous mediator of cardio-protection.[1]
The role of NO in the myocardium during conditions of low oxygen supply has become a fast-growing field of interest in basic cardiovascular research. [4] From the literature, it appears that the majority of evidence points to a protective/beneficial role for NO against the injurious effects of myocardial ischaemia, which should be of great interest to clinicians constantly in search of new cardioprotective therapies.[1]
The role of NO as a major signalling molecule in the heart and blood vessels is important and very relevant, not only to the field of basic medical sciences but also to clinical cardiology. Most experts agree that NO is by and large a potent and effective agent of cardioprotection.[1]
References:
Vascular Support
[1] Nitric oxide in the cardiovascular system: a simple molecule with complex actions. Hans Strijdom, Nontuthuko Chamane, Amanda Lochner Cardiovasc J Afr. 2009 Oct; 20(5): 303–310. PMCID: PMC3721819
[2] Endothelium-derived relaxing factor produced and released from artery and vein is nitric oxide. Ignarro LJ, Buga GM, Wood KS, Byrns RE, Chaudhuri G Proc Natl Acad Sci U S A. 1987 Dec; 84(24):9265-9.
[3] Vascular consequences of endothelial nitric oxide synthase uncoupling for the activity and expression of the soluble guanylyl cyclase and the cGMP-dependent protein kinase. Münzel T, Daiber A, Ullrich V, Mülsch A Arterioscler Thromb Vasc Biol. 2005 Aug; 25(8):1551-7.
[4] Cardioprotective function of inducible nitric oxide synthase and role of nitric oxide in myocardial ischemia and preconditioning: an overview of a decade of research. Bolli R. J Mol Cell Cardiol. 2001 Nov; 33(11):1897-918.
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