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Titolo:
ROLE OF NON-NITRIC OXIDE NON-PROSTAGLANDIN ENDOTHELIUM-DERIVED RELAXING FACTOR(S) IN BRADYKININ VASODILATION
Autore:
RESENDE AC; BALLEJO G; SALGADO MCO;
Indirizzi:
UNIV SAO PAULO,FAC MED RIBEIRAO PRETO,DEPT FARMACOL,AV BANDEIRANTES 3900 BR-14049900 RIBEIRAO PRET SP BRAZIL UNIV SAO PAULO,FAC MED RIBEIRAO PRETO,DEPT FARMACOL BR-14049900 RIBEIRAO PRET SP BRAZIL
Titolo Testata:
Brazilian journal of medical and biological research
fascicolo: 9, volume: 31, anno: 1998,
pagine: 1229 - 1235
SICI:
0100-879X(1998)31:9<1229:RONONE>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
ARACHIDONIC-ACID METABOLITE; EDHF-MEDIATED RELAXATION; ARTERIAL SMOOTH-MUSCLE; RAT HEPATIC-ARTERY; DEPENDENT HYPERPOLARIZATION; RESISTANCE ARTERIES; MESENTERIC-ARTERY; CORONARY-ARTERIES; L-ARGININE; POTASSIUM CHANNELS;
Keywords:
PROSTAGLANDIN; BRADYKININ; NITRIC OXIDE; CYTOCHROME P450; POTASSIUM CHANNELS; ENDOTHELIUM-DEPENDENT VASODILATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
58
Recensione:
Indirizzi per estratti:
Citazione:
A.C. Resende et al., "ROLE OF NON-NITRIC OXIDE NON-PROSTAGLANDIN ENDOTHELIUM-DERIVED RELAXING FACTOR(S) IN BRADYKININ VASODILATION", Brazilian journal of medical and biological research, 31(9), 1998, pp. 1229-1235

Abstract

The most conspicuous effect of bradykinin following its administration into the systemic circulation is a transient hypotension due to vasodilation. In the present study most of the available evidence regarding the mechanisms involved in bradykinin-induced arterial vasodilation is reviewed, It has become firmly established that in most species vasodilation in response to bradykinin is mediated by the release of endothelial relaxing factors following the activation of B-2-receptors, Although in some cases the action of bradykinin is entirely mediated by the endothelial release of nitric oxide (NO) and/or prostacyclin (PGI(2)), a large amount of evidence has been accumulated during the last 10 years indicating that a non-NO/PGI(2) factor accounts for bradykinin-induced vasodilation in a wide variety of perfused vascular beds and isolated small arteries from several species including humans. Since the effect of the non-NO/PGI(2) endothelium-derived relaxing factor is practically abolished by disrupting the K+ electrochemical gradient together with the fact that bradykinin causes endothelium-dependent hyperpolarization of vascular smooth muscle cells, the action of such factor has been attributed to the opening of K+ channels in these cells, The pharmacological characteristics of these channels are not uniform among the different blood vessels in which they have been examined, Although there is some evidence indicating a role for K-Ca or K-V channels, our findings in the mesenteric bed together with other reports indicate that the K+ channels involved do not correspond exactly to any ofthose already described. In addition, the chemical identity of such hyperpolarizing factor is still a matter of controversy. The postulatedmain contenders are epoxyeicosatrienoic acids or endocannabinoid agonists for the CB1-receptors. Based on the available reports and on datafrom our laboratory in the rat mesenteric bed, we conclude that the NO/PGI(2)-independent endothelium-dependent vasodilation induced by BK is unlikely to in involve a cytochrome P450 arachidonic acid metabolite or an endocannabinoid agonist.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/09/20 alle ore 09:32:05