ATP stimulated cyclic AMP formation in bovine chromaffin cells is enhanced by neuropeptide Y

ATP increases cAMP formation in bovine chromaffin cells, EC(50) = 7.1 x 10(-6) M. NPY, EC(50) = 4.1 x 10(-8) M, increases the efficacy of ATP (1.5-2 fold). Inclusion of the selective Y1 receptor antagonist 1229U91 produced a decrease in NPY potency (EC(50) = 2.7 x 10(-7) M). PTX pretreatment did not abolish either the effect of ATP nor the enhancement by NPY. NPY could also enhance the ability of angiotensin and bradykinin to increase cAMP formation. The selective phospholipase C inhibitor, U73122, and the selective protein kinase C inhibitors, bisindolylmaleimide I and RO-31-8425, were effective inhibitors of the enhancing effect of NPY.

[1]  Peijin Zhang,et al.  Identification of an NPY-Y1 receptor subtype in bovine chromaffin cells , 2000, Regulatory Peptides.

[2]  J. Dickenson,et al.  Role of G-protein beta gamma subunits in the augmentation of P2Y2 (P2U)receptor-stimulated responses by neuropeptide Y Y1 Gi/o-coupled receptors. , 1997, The Biochemical journal.

[3]  J. Hurley,et al.  Catalytic mechanism and regulation of mammalian adenylyl cyclases. , 1998, Molecular pharmacology.

[4]  F. Fitzpatrick,et al.  Selective inhibition of receptor-coupled phospholipase C-dependent processes in human platelets and polymorphonuclear neutrophils. , 1990, The Journal of pharmacology and experimental therapeutics.

[5]  H Herzog,et al.  XVI. International Union of Pharmacology recommendations for the nomenclature of neuropeptide Y, peptide YY, and pancreatic polypeptide receptors. , 1998, Pharmacological reviews.

[6]  P. Parker,et al.  Isoenzyme specificity of bisindolylmaleimides, selective inhibitors of protein kinase C. , 1993, The Biochemical journal.

[7]  B. Conklin,et al.  Hormonal stimulation of adenylyl cyclase through Gi-protein βγ subunits , 1992, Nature.

[8]  J. Merritt,et al.  Different sensitivities of neutrophil responses to a selective protein kinase C inhibitor Ro 31-8425; redundancy in signal transduction. , 1997, Cellular signalling.

[9]  Martin J. Lohse,et al.  Crosstalk between Gαi- and Gαq-coupled receptors is mediated by Gβγ exchange , 1999 .

[10]  J. Zheng,et al.  Neuropeptide Y enhances ATP-induced formation of inositol phosphates in chromaffin cells. , 1997, Biochemical and Biophysical Research Communications - BBRC.

[11]  J. Leban,et al.  High-affinity neuropeptide Y receptor antagonists. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[12]  T. Hexum,et al.  Neuropeptide Y release from the adrenal medulla after cholinergic receptor stimulation. , 1987, The Journal of pharmacology and experimental therapeutics.

[13]  Y. Wong,et al.  Gi-mediated stimulation of type II adenylyl cyclase is augmented by Gq- coupled receptor activation and phorbol ester treatment , 1996, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[14]  T. Hexum,et al.  Neuropeptide Y inhibits forskolin-stimulated adenylate cyclase in bovine adrenal chromaffin cells via a pertussis toxin-sensitive process. , 1992, The Journal of pharmacology and experimental therapeutics.

[15]  Y. Kataoka,et al.  Release of NPY-like immunoreactive material from primary cultures of chromaffin cells prepared from bovine adrenal medulla , 1985, Neuropharmacology.