Evidence supporting the use of: Nitric Oxide
For the health condition: Arteriosclerosis

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Synopsis

Source of validity: Scientific
Rating (out of 5): 3

Nitric oxide (NO) is scientifically validated as a therapeutic agent relevant to arteriosclerosis, primarily due to its crucial role in vascular biology. Arteriosclerosis is characterized by thickening and stiffening of arterial walls, often associated with endothelial dysfunction. Nitric oxide, synthesized endogenously by endothelial cells via nitric oxide synthase (eNOS), is a potent vasodilator and inhibitor of platelet aggregation, leukocyte adhesion, and smooth muscle proliferation. These effects collectively help maintain vascular homeostasis and limit the progression of arteriosclerosis.

Several clinical studies demonstrate that impaired NO bioavailability is linked to endothelial dysfunction, a key early event in arteriosclerosis. Agents that increase NO synthesis or mimic its effects—such as nitrates, phosphodiesterase inhibitors, or L-arginine supplements—have shown improvement in endothelial function in both animal models and human subjects. Moreover, statins and ACE inhibitors, commonly used in cardiovascular medicine, partly exert their beneficial effects through enhancing NO production.

However, direct supplementation with nitric oxide donors is not a standard treatment for arteriosclerosis itself, but rather for symptom relief in related conditions (e.g., angina). The therapeutic focus is more on restoring endogenous NO balance rather than exogenous NO administration. Thus, while the scientific rationale is strong and evidence for mechanisms is robust, direct clinical outcome data for treating arteriosclerosis with NO donors are moderate.

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