自1987年發現內皮細胞釋放一氧化氮,且其生成由精胺酸以獨特之生化反應而來。一氧化氮由一族的一氧化氮合成酶催化生成並參與了許多生理反應。在血管內皮細胞的生成維持血管舒張張力,是血流及血壓調節之重要因素。一氧化氮在內皮或血小板中生成可抑制血小板凝集和黏著,及抑制白血球黏著並調節平滑肌細胞的增生。一氧化氮在中樞神經系統的神經元內生成,它扮演著各種生理功能的神經調節物質,包括記憶的形成。在週邊神經系統,一氧化氮是神經網路釋放的調控者,初期被認為非-腎上腺及非-膽鹼激素系統。這些神經功能控制了神經性的血管舒張作用,並影響了某些腸胃道、呼吸道及泌尿道功能。而一氧化氮不正常的生成及作用,可能導致各種臨床現象,如高血壓、動脈硬化、射精功能異常及神經退化症。此外,一氧化氮在宿主-防禦及發炎反應中會大量生成,此大量釋放作用對於某些病理發生扮演重要貢獻,包括敗血性休克及各種形式之發炎現象。因此,一氧化氮不僅是生理功能之調控者亦是病理作用之實質影響者。
The discovery in 1987 that endothelial cells release nitric oxide (NO) and the subsequent indentification of its generation from the amino acid L-arginine revealed the existence of a ubiquitous biochemical pathway. NO is formed by a family of enzymes, the NO synthases, and is involved in many physiological functions. Its formation in vascular endothelial cells maintains a vasodilator tone that is essential for the regulation of blood flow and pressure. NO produced by the endothelium and/or platelets also inhibits platelet aggregation and adhesion, inhibits leukocyte adhesion and modulates smooth muscle cell proliferation. NO is also synthesized in neurons of the central nervous system, where it acts as a neuromediator with several physiological functions, including the formation of memory, and central cardiovascular regulation. In the peripheral nervous system, NO is now known to be the mediator released by a widespread network of nerves, previously recognized as non-adrenergic and non-cholinergic. These nerves mediate some forms of neurogenic vasodilation and regulate certain gastrointestinal, respiratory and genitourinary function. Abnormal generation or action of NO contributes to a variety of clinical conditions, including hypertension, atherosclerosis, erectile dysfunction and neurodegeneration. In addition, NO is generated in large quantities during host defence and immunological reactions. NO released in this way contributes to the development of certain pathologies, including septic shock and some forms of inflammation. Thus, NO can act both as a physiological mediator and as a pathological entity.