New concepts in medicine Nitric oxide and cardiovascular disease
نویسندگان
چکیده
Accepted 25 September 1996 Traditionally, the endothelium had been regarded simply as a passive barrier lining blood vessels. However, in 1980, Furchgott and Zawadski elegantly demonstrated that the endothelium was important in vascular relaxation by releasing an endothelium-derived relaxing factor (EDRF). 1 The precise identity ofEDRF remained elusive until 1987 when Palmer et al showed that EDRF was the simple diatomic molecule nitric oxide (NO).2 Since then there has been an explosion of research in this field. It is now accepted that, among its many roles, NO is an important regulatory molecule in cardiovascular function, maintaining tone in normal blood vessels.3 NO is synthesised in vascular endothelial cells from the abundant amino acid L-arginine by the enzyme endothelial nitric oxide synthase (eNOS). The enzyme is constitutively expressed, and is therefore always present in endothelial cells. However, its activity is tightly controlled by intracellular calcium levels.4 Endothelium-dependent vasodilators such as acetylcholine act by increasing intracellular calcium, thereby increasing eNOS activity and thus NO release. eNOS belongs to a family of isoenzymes which also includes the inducible form (iNOS) which is not normally present in cells, but can be induced in vascular smooth muscle cells, macrophages and other tissues by cytokines and bacterial endotoxin. The third member of the family is brain NOS (bNOS), another constitutively expressed, calcium-dependent, isoform found in the brain and peripheral nervous system (table 1, see ref 5 for review). The NO produced by vascular endothelial cells diffuses to the smooth muscle layer where it stimulates the enzyme soluble guanylate cyclase (sGC) to produce cyclic guanosine monophosphate (cGMP) and causes vasorelaxation (figure 1). Endothelium-derived NO can be stimulated by shear stress on the endothelial cells caused by increased blood flow. This is thought to be one of the mechanisms whereby physical exercise improves endothelial function and cardiovascular function in general.6
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