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Extracellular Sodium Dependence of GnRH‐Stimulated Growth Hormone Release in Goldfish Pituitary Cells
Author(s) -
Van Goor Fredrick,
Goldberg Jeffrey I.,
Chang John P.
Publication year - 1997
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1046/j.1365-2826.1997.00572.x
Subject(s) - extracellular , medicine , endocrinology , veratridine , gonadotropin releasing hormone , protein kinase c , chemistry , stimulation , depolarization , tetrodotoxin , antiporter , sodium , sodium channel , biology , hormone , kinase , luteinizing hormone , biochemistry , organic chemistry
In goldfish, gonadotropin‐releasing hormone (GnRH) stimulation of growth hormone (GH) release has been shown to involve extracellular Ca 2+ entry through voltage‐sensitive Ca 2+ channels and the activation of protein kinase C (PKC). In this study, the possible involvement of extracellular Na + in mediating the GH response to GnRH was examined using dispersed pituitary cells. Perifusion with Na + ‐depleted medium reversibly reduced the acute GH response to 5‐min pulses of either 10 nM salmon (s)GnRH or 10 nM chicken (c)GnRH‐II. Similarly, replacement of normal medium with Na + ‐depleted medium attenuated the long‐term GH release response to sGnRH and cGnRH‐II under static incubation conditions. These results suggest that GnRH‐induced GH release requires the presence of extracellular Na + . Treatment with 5‐min pulses of the Na + ‐channel agonist veratridine (10 μM) increased GH release in an extracellular Ca 2+ ‐dependent manner, presumably due to activation of voltage‐sensitive Ca 2+ channels resulting from the depolarizing effect of increased Na + influx. On the other hand, Na + entry through tetrodotoxin (TTX)‐sensitive, voltage‐dependent Na + channels is not involved in GnRH‐induced GH release. Application of 250 nM TTX, which abolished the voltage‐sensitive Na + currents in identified goldfish somatotropes, did not affect the acute GH responses to 5‐min pulses of sGnRH and cGnRH‐II. The possible participation of Na + /H + antiport in mediating the extracellular Na + ‐dependent GnRH action on GH release was then examined. In static incubation experiments, sGnRH‐ and cGnRH‐II‐induced GH secretion were reduced by inhibitors of the Na + /H + antiport, amiloride and dimethylamiloride (DMA). Likewise, the GH response to the PKC activator, tetradecanoyl phorbol acetate, was attenuated by treatment with Na + ‐depleted medium, amiloride, and DMA. The inhibitory actions of amiloride and DMA were selective as these drugs did not affect the GH response elicited by the Ca 2+ ionophore ionomycin and the voltage‐sensitive Ca 2+ channel agonist, Bay K 8644. Taken together, these results indicate that extracellular Na + and the Na + /H + exchanger are involved in the mediation of GnRH‐stimulated GH release in goldfish. Furthermore, this dependence on Na + and Na + /H + antiport probably occurs distal to the activation of PKC by GnRH.