Disorders of the circulatory system – vascular diseases – are common in the developed world, and can lead to heart attacks, strokes and even death. However, treatments for these disorders, such as bypass surgery and angioplasty, themselves induce vascular injury, after which the cells of the blood vessel can over-proliferate in a way that limits blood flow. Nitric oxide (NO) is an important molecule that helps maintain the contractility and health of vascular smooth muscle cells, and multiple studies have linked vascular pathology to a decreased level of NO. Therefore, therapies that increase the availability of NO could help protect vascular health.

NO is synthesized from arginine (an amino acid) by an enzyme called endothelial nitric oxide synthase (NOS). In new research, Brian Zuckerbraun and colleagues, of the University of Pittsburgh, in Pittsburgh, Pennsylvania, determined that after vessel injury in the rat, the NOS pathway is disrupted, but a secondary pathway that generates NO from nitrate is activated. Furthermore, supplementing rats with dietary nitrate before inducing vessel injury markedly limited the extent of the damage, while a diet low in nitrate exacerbated it. In the accompanying commentary, John Cooke and Yohannes Ghebremariam of Stanford University in Stanford, California point out that high levels of dietary nitrate might in part explain the vascular benefits of diets rich in leafy greens (spinach, lettuce, and beets are nitrate-rich), but warn that high dose supplementation could lead to the generation of carcinogenic molecules (Courtesy of EurekAlert!, a service of AAAS).

The complete article is available free online here:

Nitrate in diet for vascular health

Commentary also available online here:

Dietary nitrate, nitric oxide, and restenosis

Reference: Matthew J. Alef, et al. Nitrite-generated NO circumvents dysregulated arginine/NOS signaling to protect against intimal hyperplasia in Sprague-Dawley rats. Published March 23, 2011. J Clin Invest. doi:10.1172/JCI44079