Calcitonin secretion and cyclic AMP-efflux from C-cells, stimulated by glucagon and either calcium or Bay K 8644.
The interaction of glucagon and either calcium or Bay K 8644 on calcitonin (CT)-release and cAMP-efflux was studied in a rat C-cell line, (rMTC 6-23). CT secretion was stimulated by glucagon up to 216%, ionized calcium (Ca++) up to 112%, and Bay K 8644 up to 81% above the control. The combination of glucagon with either Ca++ or Bay K 8644 resulted in an additive effect. cAMP-efflux was grossly incremented by glucagon (536 pmol/mg), slightly by Ca++ (11.6 pmol/mg) and not at all by Bay K 8644 (less than 3 pmol/mg). The combination of glucagon with either calcium or Bay K 8644 caused a reduction of the cAMP-increase obtained by glucagon alone. These data suggest complex interactions between the cAMP and the intracellular calcium-dependent pathway, but an additive effect of the two pathways on CT-release.
Scherübl
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H
Abteilung Innere Medizin I, Universität Heidelberg, Germany.
Raue
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F
Zopf
G
G
Ziegler
R
R
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology*; D000818:Animals; D002116:Calcitonin / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology*; D002277:Carcinoma / Q000378:metabolism / Q000473:pathology*; D002460:Cell Line; D000242:Cyclic AMP / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D005934:Glucagon / Q000494:pharmacology*; D051381:Rats; D013961:Thyroid Gland / Q000166:cytology*; D013964:Thyroid Neoplasms / Q000378:metabolism / Q000473:pathology*; D014407:Tumor Cells, Cultured / Q000378:metabolism / Q000473:pathology
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D002116:Calcitonin; D005934:Glucagon; D000242:Cyclic AMP; D002118:Calcium