Tobias Esch, George B Stefano, Gregory L Fricchione, Herbert Benson
Med Sci Monit 2002; 8(6): RA103-118
Nitric oxide (NO) is involved in stress physiology and stress-related diseaseprocesses. Like stress, NO seems to be capable of principally exerting either beneficial or deleteriouseffects. The actual distinction depends on a multitude of factors. Moreover, NO counteracts norepinephrine(NE) activity and sympathetic responsivity. Thus, NO and the stress (patho)physiology are closely connectedand molecular mechanisms or pathways may be shared under certain conditions. NO is involved in immunological,cardiovascular, and neurodegenerative diseases/ mental disorders. It represents a 'double-edged sword',since small quantities produced by constitutive enzymes may predominantly mediate physiological effects,whereas the expression of inducible NO synthases may lead to larger quantities of NO, a situation thatmay be associated with cytotoxic and detrimental effects of NO. The key step for normally useful physiologicalmechanisms becoming pathophysiological may be represented by the loss of balance, the loss of controlover the different pathways induced. A failure to terminate or shift originally protective mechanismsmay lead to a vicious cycle of disease-supporting pathophysiological pathways.CONCLUSIONS: Profound connectionsbetween stress and various disease processes exist. Thereby, common pathophysiological pathways in stress-relateddiseases have been described, and they involve stress hormone (cortisol, NE) and, in particular, NO activity.Thus, NO has detrimental capacities. However, NO not only exerts deleterious but also strongly amelioratingeffects. The balance between both properties is crucial. Yet, nitric oxide involvement in stress-relateddiseases represents a common pathway, with various pathophysiological analogies, that may be accessiblefor strategies using stress management and relaxation response techniques.
Keywords: Cardiovascular Diseases, Mental Disorders, Neurodegenerative Diseases, Nitric Oxide, Research Support, Non-U.S. Gov, Research Support, U.S. Gov, Signal Transduction, Stress