Mechanisms of isoproterenol-induced atrial natriuretic peptide release from superfused rabbit atria

• Published in: The American journal of physiology Vol. 265; no. 4 Pt 2; p. H1283
• Main Authors: Azizi, C, Carayon, A, Masson, F, Noé, E, Barthelemy, C, Eurin, J, Maistre, G, Legrand, J C
• Format: Journal Article
• Language: English
• Published: United States 01.10.1993
• Subjects: Animals; Atrial Natriuretic Factor - metabolism; Calcium - pharmacology; Cyclic AMP - metabolism; Heart Atria; In Vitro Techniques; Isoproterenol - pharmacology; Myocardium - metabolism; Norepinephrine - pharmacology; Perfusion; Rabbits
• ISSN: 0002-9513
• DOI: 10.1152/ajpheart.1993.265.4.h1283

The mechanisms for isoproterenol-induced atrial natriuretic peptide (ANP) release were studied in superfused rabbit sliced right atria. Addition of 1 microM norepinephrine to this preparation induced a significant monophasic twofold rise in ANP release. This effect was abolished by 1 microM propranolol and mimicked by 1 microM isoproterenol. Furthermore, addition of 200 microM 3-isobutyl-1-methylxanthine (IBMX) to the superfusing medium potentiated isoproterenol effect 31%. In addition, superfusion of slices with 0.5 mM N6,2-O-dibutyryladenosine 3',5'-cyclic monophosphate [(Bu)-2cAMP] enhanced ANP release in the same manner as the beta-agonist. After isoproterenol stimulation, adenosine 3',5'-cyclic monophosphate (cAMP) concentration in effluents increased significantly. ANP secretory response to isoproterenol was unaffected by extracellular calcium concentration or 1 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA). Finally, 10 microM indomethacin significantly reduced isoproterenol-stimulated ANP release. It is concluded that 1) norepinephrine-induced ANP release is mediated by its beta-agonist activity, 2) isoproterenol-stimulated release appears to be mediated by cAMP, 3) isoproterenol effect does not require extracellular calcium, and 4) prostaglandins may be involved in this beta-adrenergic effect.