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Titolo:
ETHANOL ENHANCES THE ENDOTHELIAL NITRIC-OXIDE SYNTHASE RESPONSE TO AGONISTS
Autore:
DAVDA RK; CHANDLER LJ; CREWS FT; GUZMAN NJ;
Indirizzi:
UNIV FLORIDA,COLL MED,DEPT PHARMACOL,JHMHC,POB 100267 GAINESVILLE FL 32610 UNIV FLORIDA,COLL MED,DEPT PHARMACOL,JHMHC,POB 100267 GAINESVILLE FL 32610 UNIV FLORIDA,COLL MED,DIV NEPHROL HYPERTENS & TRANSPLANTAT GAINESVILLE FL 32610
Titolo Testata:
Hypertension
fascicolo: 6, volume: 21, anno: 1993,
parte:, 2
pagine: 939 - 943
SICI:
0194-911X(1993)21:6<939:EETENS>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
VASCULAR SMOOTH-MUSCLE; ALCOHOL; HYPERTENSION; RELAXATION; ACETALDEHYDE; TOLERANCE; ACETATE; CALCIUM; CELLS;
Keywords:
ETHANOL; ENDOTHELIUM; NITRIC OXIDE; ENDOTHELIUM-DERIVED RELAXING FACTOR; HYPERTENSION, ETHANOL-RELATED;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
27
Recensione:
Indirizzi per estratti:
Citazione:
R.K. Davda et al., "ETHANOL ENHANCES THE ENDOTHELIAL NITRIC-OXIDE SYNTHASE RESPONSE TO AGONISTS", Hypertension, 21(6), 1993, pp. 939-943

Abstract

Chronic ethanol consumption is associated with an increased prevalence of hypertension. The mechanisms of this form of hypertension are unknown. Rats fed ethanol for 2 days develop a tolerance to the acute vasoconstrictive effects of ethanol that is believed to be endothelium dependent. We investigated the effects of acute and chronic ethanol exposure on agonist-stimulated nitric oxide synthase activity in bovine pulmonary artery endothelial cells. Exposure of bovine pulmonary artery endothelial cells to ethanol (100 mmol/L) for 20-120 minutes did not change either basal or agonist-stimulated nitric oxide synthase activity measured as the rate of conversion of [H-3]L-arginine to [H-3]L-citrulline. Chronic exposure of endothelial cells to ethanol (100 mmol/L) for 96 hours significantly increased bradykinin-, adenosine 5'-triphosphate-, and ionomycin-stimulated nitric oxide synthase activity without affecting basal enzyme activity. The ethanol-induced increase in nitric oxide synthase response to agonists was dependent on the duration of ethanol exposure as well as the concentration of ethanol. Moreover,the effect of ethanol was characterized by an increase in the maximalnitric oxide synthase response to adenosine 5'-triphosphate without changes in the EC50. Removal of calcium or addition of N-nitro-L-arginine completely abolished agonist-stimulated nitric oxide synthase activity in both control and ethanol-treated cells. Our observations support the hypothesis that ethanol enhances nitric oxide synthase response to agonists during early ethanol exposure and may serve in a protective role against its hypertensive effect.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/12/20 alle ore 18:05:57