CONFERENCE INFORMATION
Meeting Objectives
Nitrite research has reached the point of breakthroughs in the understanding of its role as a "hypoxic buffer" regulating vasodilation, cellular biology, and mitrochrondrial respiration, and modulating ischemic tissue injury. In addition, nitrite-based therapeutics offer promise in the treatment of a wide variety of human diseases characterized by tissue ischemia and regional or systemic hypoxia. It is now appreciated that the nitrite anion, found in plasma, erythrocytes, and other tissues, is converted to nitric oxide (NO) during physiological hypoxia and acidosis through a variety of mechanisms spanning the entire spectrum of low-oxygen states. This may modulate vasodilation, metabolism, and oxygen use during hypoxia. The central question has been whether this reaction occurs under physiological conditions, i.e., whether nitrite found in the body is a bioavailable pool for graded conversion to NO under hypoxic conditions. Evidence of nitrite's abundance in relevant tissues, its relative stability, and, particularly, its selective reaction with deoxyhemoglobin, deoxymyoglobin and other oxygen-binding heme proteins suggests that it is indeed a major vascular storage pool of NO. Recent studies reveal that inorganic nitrate can be a major source of nitrite and NO. This is highly interesting from a nutritional aspect since nitrate is abundant in our everyday diet. The emerging role of the Nitrate-Nitrite-NO pathway in physiology and therapautics will be discussed at the meeting.
