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NEUROHUMORAL CONTROL OF CIRCULATION AND HYPERTENSION

Cytochrome P-450 metabolites in endothelin-stimulated cardiac hormone secretion

Department of Physiology and Biophysics and the University of South Florida, Cardiac Hormone Center, Tampa, Florida 33612

Submitted 22 August 2003 ; accepted in final form 6 January 2004

We examined the role of cytochrome P-450-arachidonate (CYP450-AA) metabolites in endothelin-1 (ET-1)-stimulated atrial natriuretic peptide (ANP) and pro-ANP-(1-30) secretion from the heart. 17-Octadecynoic acid (17-ODYA, 10^-5 M) significantly inhibited ANP secretion stimulated by ET-1 (10^-8 M) in the isolated perfused rat atria and inhibited pro-ANP-(1-30) secretion stimulated by ET-1 (10^-8 M) or 20-hydroxyeicosatetraenoic acid in cultured neonatal rat ventricular myocytes (NRVM). In NRVM, 17-ODYA significantly (P < 0.05) increased secretion of cAMP but had no significant effect on the secretion of cGMP from NRVM. Staurosporine, an inhibitor of protein kinase C, completely blocked the inhibitory action of 17-ODYA, whereas a protein kinase A inhibitor, H-89 (5 x 10^-5 M), did not significantly attenuate the effects of 17-ODYA. The results show that the inhibitory action of 17-ODYA on ET-1-augmented ANP secretion is mediated through cAMP and suggest that CYP450-AA may play an important role in ET-1-induced cardiac hormone secretion.

endothelin-1; 20-hydroxyeicosatetraenoic acid; 17-octadecynoic acid; nitric oxide; protein kinase A; protein kinase C; atrial natriuretic peptide; pro-ANP-(1-30); cardiac hypertrophy

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