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Titolo:
New issues about nitric oxide and its effects on the gastrointestinal tract
Autore:
Martin, MJ; Jimenez, MD; Motilva, V;
Indirizzi:
Univ Sevilla, Fac Pharm, Dept Pharmacol, E-41012 Seville, Spain Univ Sevilla Seville Spain E-41012 ept Pharmacol, E-41012 Seville, Spain
Titolo Testata:
CURRENT PHARMACEUTICAL DESIGN
fascicolo: 10, volume: 7, anno: 2001,
pagine: 881 - 908
SICI:
1381-6128(200107)7:10<881:NIANOA>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
NONSTEROIDAL ANTIINFLAMMATORY DRUGS; GASTRIC-MUCOSAL INJURY; ISCHEMIA-REPERFUSION INJURY; INFLAMMATORY-BOWEL-DISEASE; PLATELET-ACTIVATING-FACTOR; N-ACETYL-PENICILLAMINE; VASCULAR SMOOTH-MUSCLE; CENTRAL-NERVOUS-SYSTEM; PROTEIN-KINASE-C; EXPERIMENTAL COLITIS;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
231
Recensione:
Indirizzi per estratti:
Indirizzo: Martin, MJ Univ Sevilla, Fac Pharm, Dept Pharmacol, P Garcia Gonzalez S-N,E-41012 Seville, Spain Univ Sevilla P Garcia Gonzalez S-N Seville Spain E-41012 Spain
Citazione:
M.J. Martin et al., "New issues about nitric oxide and its effects on the gastrointestinal tract", CUR PHARM D, 7(10), 2001, pp. 881-908

Abstract

Over the last years the important role of nitric oxide (NO) as endogenous modulator of numerous physiological functions has been shown. NO is involved in the regulation of blood flow, maintenance of vascular tone, control ofplatelet aggregation, and modulation of the activity of the mastocytes. Italso plays a key role as neurotransmitter in the central and peripheric nervous system (non adrenergic non colinergic, NANC, neurons), in the nervouscontrol of the cerebral blood flow and in the neuroendocrine regulation orsynaptic plasticity. However, NO shows a dual behavior: at physiological concentrations, released through the constitutive synthase (cNOS), it regulates house-keeping functions, whereas its overproduction by the inducible isoenzyme (iNOS) exhibits cytotoxic activity because interacting with reactive species producing peroxinitrites (ONOO.) and other compounds, which are highly damaging for the tissues. In the gastrointestinal tract (GIT) NO participates in the modulation of the smooth musculature tone, such as the regulation of intestinal peristaltism, gastric emptying and antral motor activity. It also regulates acid and gastric mucus secretion, alkaline production, and is involved in the maintenance of mucosal blood flow. In physiological conditions, NO acts as an endogenous mediator modulating both, the repairing and integrity of the tissues, and exhibits gastroprotective properties against different types of aggressive agents. However, high concentrations of NO are related to numerous pathological processes of GIT including peptic ulcer, chronic gastritis, gastrointestinal cancer, bacterial gastroenteritis, celiac or chronic inflammatory bowel diseases. Recently, this hypothesis that cNOS is always beneficial and iNOS is always deleterious, has been questioned, since that a seriesof data suggest that the increase of cNOS activity could be responsible for the derived pathological changes and, by contrast, NO liberated by the inducible isoenzyme might play a repairing effect in certain pathological disorders. The pharamceutical industry is really interested in proving the clinical benefits of the mediator. Numerous NO-donor drugs, nitrite derivatives, havebeen frequently used in the cardiovascular diseases due to their vasodilating properties, which allow an enhancement of coronary blood flow. More recently, the protective effect of NO against non-steroidal antiinflammatory drugs (NSAID)-gastroenteropathy has been shown, because its vasodilating andantioxidant properties render it a potentially useful agent. Different NSAID, including acetyl salicylic acid, diclofenac or naproxen, have been formulated by attaching a NO releasing-moiety. These NO-NSAID, antiinflammatories combined with precursors of the mediator, or with inhibitors of the inducible synthase, are currently being evaluated. However, although the pharmacotherapeutical possibilities of NO are considerable, it is necessary to elucidate the exact mechanisms derived from simulation/inhibition of the isoenzymes in order to determine the clinical utility of NO-donors.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/01/20 alle ore 21:27:15