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Endocrinology, Vol 110, 910-915, Copyright © 1982 by Endocrine Society


ARTICLES

Effects of somatostatin and urotensin II on tilapia pituitary prolactin release and interactions between somatostatin, osmotic pressure Ca++, and adenosine 3',5'-monophosphate in prolactin release in vitro

EG Grau, RS Nishioka and HA Bern

Both somatostatin (SRIF) and urotensin II, a dodecapeptide from the teleost caudal neurosecretory system, inhibit PRL release from the organ-cultured rostral pars distalis of the tilapia, Sarotherodon mossambicus, in a dose-related manner. The inhibitory action of SRIF on PRL release was completely prevented by the presence of the calcium ionophore A23187. PRL release was also blocked when Ca++ was excluded from the incubation medium, even in the presence of the ionophore. Both dibutyryl cAMP (dbcAMP) and the phosphodiesterase inhibitor 3-isobutyl- 1-methylxanthine, alone or in combination, stimulated PRL release during incubation in high osmotic pressure medium. The effect of dbcAMP appeared to be dose related. Together, dbcAMP and 3-isobutyl-1- methylxanthine were also effective in preventing the inhibition of PRL release by SRIF. These results are consistent with the notion that Ca++, and possibly cAMP, may be important mediators of PRL secretion, and it is likely that SRIF may inhibit PRL release by blocking a Ca++- or cAMP-mediated mechanism.


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Am. J. Physiol. Cell Physiol.Home page
A. P. Seale, N. H. Richman III, T. Hirano, I. Cooke, and E. G. Grau
Cell volume increase and extracellular Ca2+ are needed for hyposmotically induced prolactin release in tilapia
Am J Physiol Cell Physiol, May 1, 2003; 284(5): C1280 - C1289.
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