Description of NO-dependent mechanisms of inflammation includes discussion of the role of macrophages and neutrophils in NO synthesis during various stages of inflammation, role of NO in hemodynamics, cytotoxic activity of NO, and function of NO in pain syndrome associated with inflammation. The available data suggest that NO can play various roles depending on its local concentration of the immunological state of the organism. Also, considering tumor cells and tissues, inhibition of HO-1 activity in tumor cells can enhance their susceptibility to chemotherapy. Finally, a complex interaction of four inducible enzymes in rheumatoid arthritis is discussed, and it is emphasized that consideration of this interaction is required for development of new therapy. The introduction includes a description of the regulation of atherosclerosis by numerous factors, this being why the etiology and pathogenesis of atherosclerosis are still unclear.
Some data indicate that formation of prostacyclin suppresses atherogenesis.
However, in atherosclerosis, prostacyclin synthesis can be disrupted on the level of prostacyclin synthase, which is inactivated by peroxynitrite. The authors suggest that iNOS and COX-2 expression in atherosclerosis is a protective response of the organism. The chapter includes a short introduction into mechanisms of angiogenesis. Sensitization of pain receptors is characteristic for all types of pain syndromes. The introduction includes a description of pain receptors, hyperalgesia, and mediators.