Key result
The nitrate/nitrite/NO pathway shows potential for treating atherosclerosis and pulmonary hypertension.
The nitrate/nitrite/NO pathway offers a potential therapeutic alternative to increase nitric oxide bioavailability in conditions characterized by vascular dysfunction.
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Supports nitrate pathway exploration in vascular dysfunction; leaves open randomized confirmation before clinical adoption.
Nitric oxide (NO) generated through L-arginine metabolism by endothelial nitric oxide synthase (eNOS) is an important regulator of the vessel wall. Dysregulation of this system has been implicated in various pathological vascular conditions, including atherosclerosis, angiogenesis, arteriogenesis, neointimal hyperplasia, and pulmonary hypertension. The pathophysiology involves a decreased bioavailability of NO within the vessel wall by competitive utilization of L-arginine by arginase and "eNOS uncoupling." Generation of NO through reduction of nitrate and nitrite represents an alternative pathway that may be utilized to increase the bioavailability of NO within the vessel wall. We review the therapeutic potential of the nitrate/nitrite/NO pathway in vascular dysfunction.
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Madigan et al. (2013) conducted a review in Vascular dysfunction. Nitrate/nitrite/NO pathway therapies was evaluated. The nitrate/nitrite/nitric oxide pathway represents a potential therapeutic alternative for delivering nitric oxide to treat vascular dysfunction, including atherosclerosis and pulmonary hypertension.
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