The phorbol ester induced atrial natriuretic peptide secretion is stimulated by forskolin and Bay K8644 and inhibited by 8-bromo-cyclic GMP |
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| Authors: | H Ruskoaho M Toth D Ganten T Unger R E Lang |
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| Affiliation: | 1. Dana-Farber Cancer Institute, Population Sciences Division, Center for Community Based Research, Boston, USA;2. Harvard TH Chan School of Public Health, Department of Social and Behavioral Sciences, Boston, USA;3. Seoul National University, Department of Communication, Seoul, Republic of Korea;4. University of Minnesota, Hubbard School of Journalism and Mass Communication, Minneapolis, USA;5. University of Illinois at Urbana-Champaign, Department of Communication, Urbana, USA;1. School of Geography, Archaeology & Environmental Studies, University of the Witwatersrand, Johannesburg 2050, South Africa;2. College of Life & Environmental Science, University of Exeter, Penryn TR10 9EZ, UK;1. Behavioral Engineering Group, Campus Leuven, Naamsestraat 69, box 3545, 3000 Leuven, Belgium;2. Behavioral Engineering Group, Naamsestraat 69, box 3545, 3000 Leuven, Belgium |
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| Abstract: | The role of intracellular signals in the regulation of atrial natriuretic peptide (ANP) release was studied using the isolated perfused rat heart. The phorbol ester, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), known to activate the protein kinase C pathway, produced a dose-dependent increase in perfusate ANP immunoreactivity. Bay k8644, a putative calcium channel activator, and forskolin, which stimulates adenylate cyclase, induced a sustained increase in ANP secretory rate. TPA in combination with either Bay k8644 or forskolin induced higher ANP secretion than the calculated additive value for each agent. 8-bromo-cyclic GMP and sodium nitroprusside, when given alone, had no effect on ANP secretion, but delayed the TPA-stimulated increase in perfusate ANP. ANP secretion appears therefore to be mediated both by the phosphoinositide and the cAMP system, whereas the cGMP pathway may be inhibitory. |
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