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Titolo:
Epoxygenase metabolites contribute to nitric oxide-independent afferent arteriolar vasodilation in response to bradykinin
Autore:
Imig, JD; Falck, JR; Wei, SZ; Capdevila, JH;
Indirizzi:
Tulane Univ, Sch Med, Dept Physiol, New Orleans, LA 70112 USA Tulane UnivNew Orleans LA USA 70112 t Physiol, New Orleans, LA 70112 USA Univ Texas, SW Med Ctr, Dept Biochem, Dallas, TX 75235 USA Univ Texas Dallas TX USA 75235 ed Ctr, Dept Biochem, Dallas, TX 75235 USA Vanderbilt Univ, Sch Med, Dept Med, Nashville, TN 37212 USA Vanderbilt Univ Nashville TN USA 37212 Dept Med, Nashville, TN 37212 USA
Titolo Testata:
JOURNAL OF VASCULAR RESEARCH
fascicolo: 3, volume: 38, anno: 2001,
pagine: 247 - 255
SICI:
1018-1172(200105/06)38:3<247:EMCTNO>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
ARACHIDONIC-ACID EPOXYGENASE; HYPERPOLARIZING FACTOR; RAT-KIDNEY; EPOXYEICOSATRIENOIC ACIDS; CORONARY-ARTERIES; CYTOCHROME-P450; EXPRESSION; INHIBITION; PROTEIN; CLONING;
Keywords:
bradykinin; nitric oxide; endothelium-derived hyperpolarizing factor cytochrome P450 metabolites epoxyeicosatrienoic acids; prostaglandins; kidney;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Imig, JD Tulane Univ, Sch Med, Dept Physiol, 1430 Tulane Ave,SL39, New Orleans, LA 70112 USA Tulane Univ 1430 Tulane Ave,SL39 New Orleans LA USA 70112 112 USA
Citazione:
J.D. Imig et al., "Epoxygenase metabolites contribute to nitric oxide-independent afferent arteriolar vasodilation in response to bradykinin", J VASC RES, 38(3), 2001, pp. 247-255

Abstract

In the kidney, epoxyeicosatrienoic acids (EETs) have been suggested to be endothelium-derived hyperpolarizing factors (EDHFs). The aim of the presentstudy wars to determine the contribution of EETs to the preglomerular vasodilation elicited by bradykinin. Sprague-Dawley rats were studied utilizingan in vitro perfused juxtamedullary nephron preparation. The afferent arteriolar diameter was determined and the diameter averaged 19 +/- 1 mum (n = 26) at a renal perfusion pressure of 100 mm Hg. Addition of 1, 10 and 100 nM bradykinin to the perfusate dose-dependently increased afferent arteriolar diameter by 5 +/- 1, 12 +/- 2 and 17 +/- 2%, respectively. The nitric oxide inhibitor NO-nitro-L-arginine reduced bradykinin-induced afferent arteriolar vasodilation by 50%, and the diameter increased by 9 +/- 2% in response to 100 nM bradykinin. Epoxygenase inhibitors N-methylsulphonyl-6-(2-propar-gyloxyphenyl)hexanamide or miconazole greatly attenuated the nitric oxide-independent component of the vasodilation elicited by bradykinin. Cyclooxygenase (COX) inhibition attenuated the nitric oxide-independent vasodilation elicited by 1 nM bradykinin but did not significantly affect the vascularresponse to 100 nM bradykinin. Combined inhibition of nitric oxide, COX and epoxygenase pathways completely abolished bradykinin-mediated afferent arteriolar vasodilation. In additional studies, renal microvessels were isolated and incubated with bradykinin and samples were analyzed by NICI/GC/MS. Under control conditions, renal microvascular EET levels averaged 49 +/- 9 pg/mg/20 min (n = 7). In the presence of bradykinin, EET levels were significantly higher and averaged 81 +/- 11 pg/mg/20 min (n = 7). These data support the concept that EETs are EDHFs and contribute to the nitric oxide-independent afferent arteriolar vasodilation elicited by bradykinin. Copyright (C) 2001 S. Karger AG. Basel.

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Documento generato il 06/04/20 alle ore 05:35:31