Year: 1997
Type: book-chapter
Abstract: The free radical nitric oxide (NO) is generated by the five electron oxidation of a guanidino nitrogen from L-arginine by a group of enzymes termed NO synthases (NOS). In the past decade, it has become clear that this simple molecular species has a remarkable chemical versatility, allowing it to participate in a variety of physiological and pathophysiological cellular processes in the lung [1]. NO has been characterized, for example, as a neurotransmitter [2], a second messenger [3, 4], a paracrine hormone [5, 6], and a cytotoxin [3, 7]. Accordingly, the production, distribution and fate of NO are tightly regulated [8–10]. Derangement of this balance may result in a state of NO deficiency or excess [11], manifested by inflammation [12–14], hypotension [15], transplant rejection [16], macromolecular epithelial hyperpermeability [17], hypertension [18], smooth muscle hyperplasia [19, 20] and ischemia/reperfusion injury [21]. Currently, clinical investigations are underway in which the level of tissue NO is pharmacologically manipulated by exogenous delivery of NO in its gaseous form or via inhibition of NO synthases. The proper application of these approaches in the treatment of pulmonary disease, as well as an understanding of their anticipated side-effects, necessitates an understanding of the physiological and pathophysiologic role of NO in the lung [3]. This review focuses on the role of nitric oxide in the lung and discusses the potential therapeutic options in the management of NO-related disease. These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
Source: Birkhäuser Basel eBooks
Authors: Csaba Szabó, Andrew L. Salzman
Institution: Cincinnati Children's Hospital Medical Center
Language: English
Subfield: Physiology
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W187548565