Pathophysiology and clinical applications of nitric oxide Gabor Rubanyi; Amsterdam; 1999; Harwood; 586 pages; $220.00. The book Pathophysiology and Clinical Applications of Nitric Oxide , edited by one of the leaders in endothelial cell research, Gabor Rubanyi, is a terrific addition to the Endothelial Cell Research series. It is dedicated to the three scientists who received the 1998 Nobel prize in medicine for discovering nitric oxide as a novel mediator of many biological functions. This is a two-part book, with part A beginning with a historical perspective on NO in biology by R. F. Furchgott. His essential observation that the endothelium was necessary to mediate vasodilation to acetylcholine began what is now a huge and growing field of NO research. Since this landmark observation, NO has been implicated not only in normal biologic function, but also in many pathophysiologic processes, including inflammatory diseases, ischemia and reperfusion injury, and reproductive diseases. Although there have been many good books written on NO, what sets this book apart from the rest is the expansion to both disease processes and therapeutic applications of NO. This is truly the way of the future for NO and an important advancement to make. It is amazing how far NO research has progressed in just the past 5 years. The first part of this book describes in detail the generation and biological actions of NO. This includes chapters that give state-of-the-art comprehensive examinations of such features as the structure/function relationships of the isoforms of NO synthase and the regulation of NO synthase gene expression, as well as the regulation of gene expression by NO. One of my favorite chapters in part A is chapter 8, “NO and the Regulation of Vasoactive Genes.” This chapter describes just how complex NO activity on biological functions can be: a decrease in oxygen tension (hypoxia) affects the synthesis and release of vasoactive substances. Nitric oxide, a vasoactive substance itself, has been shown to affect the genes that encode these hypoxia-induced substances. In other words, NO can act as a feedback molecule and modulate hypoxia-induced signals. These findings go beyond our classic thinking that NO acts alone during hypoxia/ischemia, because there appear to be crucial interactions among NO, gene expression, and hypoxia that may help explain disease processes such as atherosclerosis, pulmonary hypertension, and systemic sclerosis. Part B of this two-part series contains two sections: one on NO and the pathophysiology of disease and one on therapeutic applications. The inclusion of these two sections makes this book stand out from others. Although not all diseases relating to NO function are covered, there are specific chapters that address many of the complications associated with NO. Several chapters that I particularly enjoyed were those that are not as prominently associated with NO such as preterm labor, rheumatoid arthritis, and multiple sclerosis. Everyone can learn from those chapters. It is also fitting and enlightening to read the last part of this book on therapeutic applications of NO. This section signifies that we have moved forward in our understanding of NO and its role in disease to the stage where we are ready to consider treatments. This includes such approaches as gene therapies either to provide necessary NO to where it is lacking (eg, by replacing deficient iNOS) or to decrease NO production during times when it is too great (eg, by NOS and peroxynitrite inhibition). I recommend this book to anyone interested in nitric oxide. doi:10.1067/mva.2000.105886