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Titolo:
Angiotensin converting enzyme protects acetylcholine-induced relaxation from its attenuation by formyl-methionyl-leucyl-phenylalanine in rat aorta
Autore:
Ando, K; Fujita, T;
Indirizzi:
Univ Tokyo, Fac Med, Dept Endocrinol & Nephrol, Bunkyo Ku, Tokyo 1128688, Japan Univ Tokyo Tokyo Japan 1128688 Nephrol, Bunkyo Ku, Tokyo 1128688, Japan
Titolo Testata:
JOURNAL OF HYPERTENSION
fascicolo: 2, volume: 19, anno: 2001,
pagine: 223 - 228
SICI:
0263-6352(200102)19:2<223:ACEPAR>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENDOTHELIAL-CELLS; NEUTRAL ENDOPEPTIDASE; VASCULAR-RESPONSES; HUMAN-NEUTROPHILS; HYPERTROPHY; CHEMOTAXIS; INHIBITION; LEUKOCYTES; PEPTIDE; ACE;
Keywords:
formyl receptor; vascular endothelial cells; captopril; dexamethasone;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
26
Recensione:
Indirizzi per estratti:
Indirizzo: Ando, K Univ Tokyo, Fac Med, Dept Endocrinol & Nephrol, Bunkyo Ku, 3-28-6 Mejirodai, Tokyo 1128688, Japan Univ Tokyo 3-28-6 Mejirodai Tokyo Japan 1128688 yo 1128688, Japan
Citazione:
K. Ando e T. Fujita, "Angiotensin converting enzyme protects acetylcholine-induced relaxation from its attenuation by formyl-methionyl-leucyl-phenylalanine in rat aorta", J HYPERTENS, 19(2), 2001, pp. 223-228

Abstract

Objective A chemotactic tripeptide formyl-methionyl-leucyl-phenylalanine (fMLP) attenuated acetylcholine (ACh)-induced relaxation. Because angiotensin converting enzyme (ACE), which inactivates fMLP, is rich in vascular endothelial cells, we examined whether endothelial cell ACE inhibits the attenuating effect of fMLP on ACh-induced relaxation. Design and methods ACh-induced relaxation was evaluated in aortic rings from 9-week-old Sprague-Dawley rats. We examined the effects of ACE, the ACE inhibitor captopril and/or fMLP on ACh-induced relaxation in aortas from rats with or without dexamethasone treatment, which enhances ACE activity,Results Pre-treatment with ACE did not alter ACh-induced relaxation in control aortas but abolished the inhibitory effect of fMLP on ACh-induced relaxation [maximal relaxation (E-max): 95.4 +/- 1.2 versus 75.5 +/- 1.9%, P < 0.05]. Conversely, captopril enhanced the attenuation of ACh-induced relaxation by fMLP (E-max: 62.5 +/- 3.3 versus 74.0 +/- 2.2%, P < 0.05), althoughcaptopril did not affect ACh-induced relaxation in control aortas. In addition, fMLP did not attenuate ACh-induced relaxation in aortas from dexamethasone-treated rats (E-max: 89.7 +/- 3.7 versus 85.2 +/- 3.8%, NS), which enhanced ACE activity of aortas (3.37 +/- 0.25 versus 2.70 +/- 0.20 IU/mg protein, P < 0.05). Conclusion Endothelial-cell ACE attenuates the effect of fMLP on ACh-induced relaxation, possibly by its cleavage. (C) 2000 Lippincott Williams & Wilkins.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/07/20 alle ore 12:48:25