Nitric Oxide and Atherosclerosis

Dr. Valentin Fuster, former president of the American Heart Association, claimed:

“The discovery of nitric oxide and its function is one of the most important in the history of cardiovascular medicine.” Even given that the discovery of nitric oxide has clarified the most basic mechanism in the body that helps prevent atherosclerosis and heart disease, scientists still haven’t harnessed the power of the “miracle cell signaling molecule.”

Atherosclerosis is the major source of morbidity and mortality in the developed world. The impact of atherosclerosis is profound and more prevalent than one might think. Atherosclerosis claims more lives than all types of cancer combined and the economic costs are staggering.

Decreased nitric oxide availability is a hallmark of atherosclerosis. Nitric oxide is a gas that’s produced in the arterial lining – the endothelium -and regulates a wide spectrum of functions in the cardiovascular system including relaxing of the arteries and preventing blood cells from clumping together.

Endothelial dysfunction (when the arterial lining doesn’t produce enough nitric oxide) is considered to be an early marker of atherosclerosis and can develop before ultrasound evidence of atherosclerotic plaque formation can be demonstrated. Many people have atherosclerosis and are completely unaware because symptoms don’t often appear until it is already at an advanced stage. Some of the signs that could be indicative of atherosclerosis are pain in the legs when walking, suddenly numb limbs, erectile dysfunction, blurry vision, headaches, and chest pain. However, signs vary depending on where in the body the greatest blockage occurs.

The concept of endothelial dysfunction arises from variations in blood flow observed in patients with atherosclerosis compared with healthy people. Impaired endothelium may abnormally reduce vascular perfusion, produce factors that decrease plaque stability, and augment the thrombotic response to plaque rupture. There are a number of studies showing that insufficient nitric oxide production from the endothelium is associated with all major cardiovascular risk factors such as: hyperlipidemia, diabetes, hypertension, and smoking and importantly also has a profound predictive value for the future progression of atherosclerotic disease.

The concern doctors have with nitric oxide supplementation and atherosclerosis is that it can exert both atherosclerotic and protective effects depending on the source of production.

Therapeutic intervention for atherosclerosis from the standpoint of endogenous nitric oxide can be focused mainly on correcting endothelial dysfunction. Oxidative stress plays the major role in the endothelial dysfunction and recently is strongly attributed to endothelial nitric oxide synthase dysfunction and the uncoupling of nitric oxide. This is important because when nitric oxide couples with certain free radicals it can become damaging. Uncoupled nitric oxide converts to a superoxide-producing enzyme and leads to reduction of the nitric oxide generation but also potentiates the pre-existing oxidative stress. This contributes significantly to atherogenesis, but when anti-oxidants are present to protect nitric oxide, this coupling is averted. This is why it’s so important that a nitric oxide supplement has the proper ratio of anti-oxidant support when combined with the triggering action of specific amino acids.

Due to the fact that atherosclerosis is a complex disease, no single mechanism can fully explain the endothelial dysfunction. However, decreased nitric oxide bioavailability with subsequent inability to initiate vasodilatation and exhibit multiple life-saving and cell repairing functions appears to play a major role in atherosclerosis.

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