Somatostatin actions on a protein kinase C-dependent growth hormone secretagogue cascade

Molecular and Cellular Endocrinology
W K Yunker, J P Chang

Abstract

In mammals, the ability of somatostatin (SS) to block growth hormone (GH) secretion is due, in part, to the inhibition of two key intracellular mediators, cAMP and Ca2+. We examined whether or not inhibition of Ca2+ signaling was mediating SS-induced inhibition basal, as well as gonadotropin-releasing hormone (GnRH; a protein kinase C (PKC)-dependent growth hormone secretagogue)-stimulated growth hormone (GH) release. Although SS reduced basal GH release from populations of pituitary cells, parallel reductions in [Ca2+]i were not observed within single, identified somatotropes. Similarly, application of GnRH and the PKC activator DiC8 elicited increases in [Ca2+]i and GH release, but abolition of the Ca2+ responses did not accompany SS inhibition of the GH responses. Surprisingly, while DiC8 potentiated SS inhibition of GH release, SS paradoxically increased DiC8-stimulated increases in [Ca2+]i. These data establish that abolition of Ca2+ signals is not a primary mechanism through which SS lowers basal, or inhibits GnRH-stimulated hormone release.

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Citations

Oct 20, 2009·General and Comparative Endocrinology·Guang-Li LiJohn P Chang
Feb 9, 2007·General and Comparative Endocrinology·Luis Fabián CanosaRichard E Peter
May 25, 2004·The Journal of Comparative Neurology·Luis Fabián CanosaRichard Ector Peter
Jan 24, 2003·American Journal of Physiology. Cell Physiology·A P SealeE G Grau
Sep 18, 2020·Molecular and Cellular Endocrinology·Luis Fabián Canosa, Juan Ignacio Bertucci

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