Growth hormone and gonadotropin secretion in the common carp (Cyprinus carpio L.): in vitro interactions of gonadotropin-releasing hormone, somatostatin, and the dopamine agonist apomorphine.

The effects of salmon gonadotropin-releasing hormone (sGnRH) and the superactive agonist [D-Arg6, Pro9NEt]-sGnRH (sGnRH-A) on growth hormone (GH) and gonadotropin (GtH) release were examined using a perifusion system for pituitary fragments of the common carp (Cyprinus carpio). Perifusion of 2-min pulses of different concentrations of sGnRH or sGnRH-A stimulated a rapid and dose-dependent increase in GH release: ED50 values for sGnRH and sGnRH-A in stimulating GH release were 2.8 +/- 0.7 and 0.5 +/- 0.1 nM, respectively, indicating that the superactivity of sGnRH-A for stimulation of GtH release also applies in induction of GH release. Exposure of the pituitary fragments to 10 nM sGnRH or sGnRH-A alone resulted in increases in GH and GtH release on a similar temporal course. Apomorphine (10, 100, and 1000 nM) significantly inhibited basal and GnRH-induced GtH release in a dose-dependent manner and significantly stimulated basal GH release; however, APO did not enhance GnRH-induced GH release. Somatostatin (100 nM) significantly blocked basal release and 10 nM sGnRH- and sGnRH-A-induced GH release, but was ineffective on GtH release. Treatment with somatostatin (100 nM) in combination with apomorphine (100 nM) caused an increase in sGnRH-induced GH release compared to treatment with somatostatin alone; whereas, on GtH there was a significant decrease in basal and GnRH-induced levels, compared to treatment with somatostatin alone. These results indicate that GH release in common carp is regulated by somatostatin as GH release inhibitor. sGnRH and sGnRH-A act as GH-releasing factors; the mechanisms by which GnRH stimulates GH and GtH secretion are independent. The dopamine agonist apomorphine stimulates GH release and inhibits GtH release directly at the pituitary level.