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Titolo:
MYOCARDIAL PRODUCTION OF PROSTAGLANDINS - ITS ROLE IN ATRIAL-NATRIURETIC-PEPTIDE RELEASE
Autore:
AZIZI C; BARTHELEMY C; MASSON F; MAISTRE GV; EURIN J; CARAYON A;
Indirizzi:
CHU PITIE SALPETRIERE,SERV BIOCHIM,91 BLVD HOP F-75634 PARIS 13 FRANCE
Titolo Testata:
European journal of endocrinology
fascicolo: 2, volume: 133, anno: 1995,
pagine: 255 - 259
SICI:
0804-4643(1995)133:2<255:MPOP-I>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT ATRIA; SECRETION; PHOSPHORYLATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
21
Recensione:
Indirizzi per estratti:
Citazione:
C. Azizi et al., "MYOCARDIAL PRODUCTION OF PROSTAGLANDINS - ITS ROLE IN ATRIAL-NATRIURETIC-PEPTIDE RELEASE", European journal of endocrinology, 133(2), 1995, pp. 255-259

Abstract

In recent years, considerable evidence has been accumulated on prostaglandins (PG) in modulating atrial natriuretic peptide (ANP) release. In the current study we investigated whether eicosanoids promote isoproterenol-induced ANP secretion from superfused rabbit sliced atria. Inclusion of the cyclooxygenase inhibitor indomethacin (10 mu mol) to the superfusing medium abolished isoproterenol-induced ANP release. Next, PGE(2), but not PGF(2 alpha), or PGI(2) (10 mu mol), increased ANP release. Furthermore, isoproterenol-induce PGE(2) formation was fully attenuated by indomethacin. Dibutyl-cAMP (0.5 mmol) had no effect on PGE(2) formation, and the protein kinase A (PKA) inhibitor H89 (20 mu mol) did not alter isoproterenol-induced PGE(2) formation. On the other hand, indomethacin led to a significant decrease in isoprotrenol-induced cAMP production. In addition, PGE(2) enhanced basal cAMP concentration in superfusates. Superfusion of sliced atria by forskolin (10 mu mol) or by dibutyl-cAMP (0.5 mmol) produced a significant rise in ANP release. Finally, H89 was ineffective on basal ANP release but abolished the increase of ANP release in response to isoproterenol or to PGE(2). We conclude that: the effect of isoproterenol on ANP release is sensitive to indomethacin and H89; PGE(2), but not PGF(2 alpha), or PGI(2), increases ANP release; isoproterenol promotes myocardial PGE(2) formation independently of adenylate cyclase and PKA activation pathways;and PGE(2)-induced ANP release is mediated by cAMP production and subsequent PKA activation. These results suggest that isoproterenol-induced ANP release appears to be mediated at least partly by PGE(2) with underlying cAMP formation and PKA activation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/20 alle ore 06:22:33