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Am J Physiol Endocrinol Metab 273: E922-E931, 1997;
0193-1849/97 $5.00
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Vol. 273, Issue 5, E922-E931, November 1997

Role of cAMP and calcium influx in endothelin-1-induced ANP release in rat cardiomyocytes

M. C. Rebsamen1, D. J. Church2, D. Morabito1, M. B. Vallotton1, and U. Lang1

1 Division of Endocrinology and Diabetology, University Hospital, and 2 Geneva Biomedical Research Institute, CH-1211 Geneva 14, Switzerland

The mechanism of endothelin-1 (ET-1)-induced atrial natriuretic peptide (ANP) release was studied in neonatal rat ventricular cardiomyocytes. These cells expressed a single high-affinity class of ETA receptor (dissociation constant = 54 ± 18 pM, n = 3), but no ETB receptors. Incubation of cardiomyocytes with ET-1 led to concentration-dependent ANP release and prostacyclin production. ET-1-induced ANP release was affected by neither protein kinase C (PKC) inhibition or downregulation nor by cyclooxygenase inhibition, indicating that ET-1-stimulated ANP secretion is not a PKC-mediated, prostaglandin-dependent process. Furthermore, ET-1 significantly stimulated adenosine 3',5'-cyclic monophosphate (cAMP) production and increased cytosolic calcium concentration in these preparations. Both ET-1-induced calcium influx and ANP release were decreased by the cAMP antagonist Rp-cAMPS, the Rp diastereoisomer of cAMP. Moreover, ET-1-induced ANP secretion was strongly inhibited in the presence of nifedipine as well as in the absence of extracellular calcium. Thus our results suggest that ET-1 stimulates ANP release in ventricular cardiomyocytes via an ETA receptor-mediated pathway involving cAMP formation and activation of a nifedipine-sensitive calcium channel.

endothelin-1; receptor; prostacyclin formation; protein kinase C downregulation; adenosine 3',5'-cyclic monophosphate antagonist; nifedipine-sensitive calcium channel; signal transduction; atrial natriuretic peptide


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