Carbamylcholine, TRH, PGF2 alpha and fluoride enhance free intracellular Ca++ and Ca++ translocation in dog thyroid cells.
Effects on Ca++ translocation and [Ca++]i were studied in dog thyroïd cell monolayers using both 45Ca++ efflux and the indicator quin-2. Carbamylcholine, a non hydrolysable analog of acetylcholine, through muscarinic receptors, and to a lesser extent TRH and PGF2 alpha increased both these parameters. [Ca++]i increased by 171, 100 and 75% respectively over a basal level of 66 +/- 17 nM (mean +/- SD). The response to carbamylcholine was biphasic. A transient increase in [Ca++]i was followed by a more sustained phase where the [Ca++]i was slightly higher than the basal level. Only the first phase was insensitive to extracellular Ca++ depletion. This phase is probably due to a release of Ca++ from an intracellular store. NaF also induced a sustained rise in [Ca++]i dependent on extracellular Ca++ and affected 45Ca++ efflux. Our data provide direct evidence of an implication of intracellular Ca++ in the response of dog thyroïd cells to all these agents.
D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002118:Calcium / Q000378:metabolism*; D002217:Carbachol / Q000494:pharmacology*; D002478:Cells, Cultured; D003593:Cytoplasm / Q000378:metabolism; D015237:Dinoprost; D004285:Dogs; D005459:Fluorides / Q000494:pharmacology*; D066298:In Vitro Techniques; D011460:Prostaglandins F / Q000494:pharmacology*; D011976:Receptors, Muscarinic / Q000187:drug effects; D013961:Thyroid Gland / Q000187:drug effects / Q000378:metabolism*; D013973:Thyrotropin-Releasing Hormone / Q000494:pharmacology*
D011460:Prostaglandins F; D011976:Receptors, Muscarinic; D013973:Thyrotropin-Releasing Hormone; D002217:Carbachol; D015237:Dinoprost; D005459:Fluorides; D002118:Calcium