|
|
|
|
P Onali, C Eva, MC Olianas, JP Schwartz and E Costa
In GH3 pituitary cell homogenates, acetylcholine (ACh) (IC50 200 nM) inhibits adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] activity in a concentration- and GTP-dependent manner. Maximal inhibition was obtained with 10 microM ACh and corresponded to approximately a 50% decrease in basal enzyme activity. ACh inhibition is antagonized by atropine and is mimicked by muscarinic receptor agonists, but not by nicotine. ACh reduces the adenylate cyclase stimulation by vasoactive intestinal peptide (VIP), without changing its EC50. In intact GH3 cells, ACh decreases the cyclic AMP content and the rate of prolactin release in a concentration-dependent manner. When the cells are simultaneously exposed to VIP and ACh, the VIP-induced increases in cyclic AMP accumulation and prolactin release are reduced by 80% and 40%, respectively. The potency of VIP is not significantly changed by the presence of ACh, and vice versa.
This article has been cited by other articles:
![]() |
M. E. Freeman, B. Kanyicska, A. Lerant, and G. Nagy Prolactin: Structure, Function, and Regulation of Secretion Physiol Rev, October 1, 2000; 80(4): 1523 - 1631. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. Y. Ho, A. Stadnicka, P. L. Prather, A. R. Buckley, L. L. Current, Z. J. Bosnjak, and W.-M. Kwok Cannabinoid CB1 Receptor-Mediated Inhibition of Prolactin Release and Signaling Mechanisms in GH4C1 Cells Endocrinology, May 1, 2000; 141(5): 1675 - 1685. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. W. Hipkin, J. Friedman, R. B. Clark, C. M. Eppler, and A. Schonbrunn Agonist-induced Desensitization, Internalization, and Phosphorylation of the sst2A Somatostatin Receptor J. Biol. Chem., May 23, 1997; 272(21): 13869 - 13876. [Abstract] [Full Text] [PDF] |
||||