cAMP produced by pituitary adenylate cyclase-activating polypeptide 27 inhibits atrial natriuretic peptide secretion in rabbit beating atria |
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Authors: | Zhang Ying Liu Li-Ping Liang Zhe-Long Li Xiang-Lan Jin Yuan-Zhe Cui Xun |
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Affiliation: | Department of Physiology, School of Basic Medical Sciences, Yanbian University, Yanji, China. |
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Abstract: | The aim of the present study was to determine the effects of increased cAMP levels in response to pituitary adenylate cyclase-activating polypeptide 27 (PACAP27) on atrial atrial natriuretic peptide (ANP) secretion in rabbit atria. A perfused beating atrial model was used in the present study and cAMP efflux and ANP levels in atrial perfusates were measured by radioimmnoassay. At 100 nmol/L, PACAP27 increased cAMP production, which resulted in subsequent inhibition of ANP secretion. Nicardipine (1.0 micromol/L), an L-type Ca2+ channel blocker, attenuated inhibition of ANP secretion by PACAP27. Staurosporine (1.0 micromol/L), a non-specific protein kinase inhibitor, and H-89 (1.0 micromol/L), a cAMP-dependent protein kinase A (PKA) inhibitor, completely blocked the inhibition of ANP secretion in response to PACAP27 but had no effect on PACAP27-induced increases in cAMP. In conclusion, the results suggest that increased cAMP levels in response to PACAP27 negatively regulate ANP secretion via the adenylate cyclase-cAMP-PKA signalling pathway in rabbit atria and that L-type Ca2+ channels may be involved, in part, in the regulation of ANP secretion by cAMP. |
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Keywords: | atrial natriuretic peptide cAMP L‐type Ca2+ channel pituitary adenylate cyclase‐activating polypeptide 27 protein kinase |
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