Medium hyperosmolarity inhibits prolactin secretion induced by depolarizing K+ in GH4C1 cells by blocking Ca2+ influx.
Medium hyperosmolarity between 300 (normal medium osmolarity) and 600 mOsm inhibited in a concentration-correlated fashion (r greater than 0.97, p less than 0.001) the rise in intracellular Ca2+ concentration ([Ca2+]i) and prolactin (PRL) secretion induced in GH4C1 cells by depolarizing 30 mM K+. [Ca2+]i concentration and PRL secretion were tightly related between 300 and 600 mOsm (r = 0.976, p less than 0.001); 50% inhibition of both occurred at 450 mOsm. Medium hyperosmolarity slowed the rate of Ca2+ influx. At 600 mOsm the rise in both [Ca2+]i and PRL secretion was abolished but PRL secretion induced by 1 microM phorbol 12-myristate 13-acetate was not significantly reduced. Our data suggest that inhibition of Ca2+ influx may be the primary mechanism by which extracellular hyperosmolarity inhibits PRL secretion induced by high medium K+ in GH4C1 cells. Depression of the Ca2+ intracellular transduction system may play a pathophysiological role in vivo in conditions such as dehydration and hypertonic coma.
Wang
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XB
Department of Medicine, Oregon Health Sciences University, Portland 97201.
Sato
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N
Greer
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MA
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002460:Cell Line; D006982:Hypertonic Solutions; D010902:Pituitary Gland / Q000166:cytology / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D011388:Prolactin / Q000037:antagonists & inhibitors / Q000378:metabolism*; D051381:Rats; D013755:Tetradecanoylphorbol Acetate
D006982:Hypertonic Solutions; D011388:Prolactin; D013755:Tetradecanoylphorbol Acetate; D011188:Potassium; D002118:Calcium