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Titolo:
TUMOR-NECROSIS-FACTOR-ALPHA INHIBITS ENDOTHELIUM-DEPENDENT RELAXATION
Autore:
GREENBERG S; XIE JM; WANG Y; CAI BQ; KOLLS J; NELSON S; HYMAN A; SUMMER WR; LIPPTON H;
Indirizzi:
LOUISIANA STATE UNIV,MED CTR,DEPT MED,PULM & CRIT CARE MED SECT,SUITE3205,1901 PERDIDO ST NEW ORLEANS LA 70112 LOUISIANA STATE UNIV,MED CTR,DEPT PHYSIOL NEW ORLEANS LA 70112 TULANE UNIV,MED CTR,DEPT SURG,CARDIOPULM LAB NEW ORLEANS LA 70113
Titolo Testata:
Journal of applied physiology
fascicolo: 5, volume: 74, anno: 1993,
pagine: 2394 - 2403
SICI:
8750-7587(1993)74:5<2394:TIER>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHASE; VASCULAR SMOOTH-MUSCLE; ACUTE LUNG INJURY; L-ARGININE; NITROGEN-OXIDES; CELLS; ENDOTOXIN; INTERLEUKIN-1; MACROPHAGES; INDUCTION;
Keywords:
NITRIC OXIDE SYNTHASE-I AND SYNTHASE-II; PROTEIN SYNTHESIS; PLATELET-ACTIVATING FACTOR; PROSTAGLANDINS; PULMONARY VASCULATURE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
38
Recensione:
Indirizzi per estratti:
Citazione:
S. Greenberg et al., "TUMOR-NECROSIS-FACTOR-ALPHA INHIBITS ENDOTHELIUM-DEPENDENT RELAXATION", Journal of applied physiology, 74(5), 1993, pp. 2394-2403

Abstract

Tumor necrosis factor-alpha (TNF-alpha) stimulates nitric oxide (NO) in vascular endothelium by induction of the enzyme NO synthase II (NOSII). We examined the effects of TNF-alpha on 1) endothelium-dependent(EDR) and endothelium-independent (EIR) relaxation and 2) contractionof bovine intralobar pulmonary arteries (BPA) and veins (BPV) in vitro. Acetylcholine (ACh), bradykinin (BK), histamine, and A23187 produced EDR of BPA contracted with a 50% effective concentration of U-46619 (15 nM), because relaxation was abolished by endothelium-rubbing and attenuated by L-N(G)-monomethylarginine (L-NMMA; 300 muM). TNF-alpha (0.00417, 0.0417, 0.417, and 1.25 mug/ml) incubated with BPA for 60 min inhibited EDR of the BPA to ACh, BK, and histamine. The effects of TNFrequired 30 min for onset. Recovery of EDR occurred 3-4 h after washout of TNF-alpha. Pentoxifylline (1 muM) did not affect ACh-induced EDRbut selectively reversed TNF-alpha-mediated inhibition of ACh-inducedEDR. TNF-alpha-mediated inhibition of EDR was not reversible by L-NMMA, an inhibitor of NOS I and NOS II, the cyclooxygenase inhibitor ibuprofen, or CV-3908 (1 muM), a platelet-activating factor antagonist. The inhibitory effect of TNF-alpha on EDR was not mediated by nonspecific sensitization of the endothelium to human protein because recombinant human granulocyte colony-stimulating factor (10, 50, and 500 x 10(3)U/ml) did not affect EDR of BPA. The effect of TNF-alpha was specificfor release of NO from the endothelium of BPA because TNF-alpha did not affect 1) EDR of BPV to ACh, BK, or ATP; 2) EIR of BPA or BPV to nitroprusside; and 3) contraction of either BPA or BPV to KCl, U-46619, histamine, norepinephrine, or serotonin. Thus TNF-alpha appears to selectively inhibit receptor-mediated EDR and NO release in BPA. TNF-alpha-mediated inhibition of EDR differs from that of L-arginine-based inhibitors and may represent an endogenous physiological mechanism of regulation of NO in the endothelium.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 20:45:33