Modulation of calcitonin secretion by modification of calcium channels?
Voltage-dependent calcium channels (VDCC) regulating Ca++ influx through the cellular plasma membrane play a major role in the Ca(++)-induced calcitonin (CT) secretion. Using rat C-cells (rMTC 6-23 cell line), we have studied the effect of repetitive stimulation by either Ca++ (2 mM) or glucagon (10 microM) or epinephrine (10 microM) on CT secretion. Following a Ca(++)-induced initial rise, CT release declined to basal levels after about four hours despite high Ca++; addition of 10 microM glucagon to the "Ca++ desensitized C-cells" yielded the normal stimulatory effect of glucagon on CT release. Repetitive stimulation with glucagon showed a constant stimulatory action over an eight-hour period. In contrast, repetitive stimulation with 10 microM epinephrine caused an initial rise followed by a gradual decline of CT release over six hours. The observed desensitization of Ca(++)-induced CT secretion may be due to a modification of VDCC in C-cells. Whether or not the desensitization of epinephrine-induced CT release occurs independently of the regulation of VDCC remains unclear.
Scherubl
H
H
Raue
F
F
Hoflich
M
M
Ziegler
R
R
D000818:Animals; D002116:Calcitonin / Q000378:metabolism*; D015220:Calcium Channels / Q000187:drug effects* / Q000502:physiology; D002478:Cells, Cultured; D004837:Epinephrine / Q000494:pharmacology*; D005934:Glucagon / Q000494:pharmacology*; D066298:In Vitro Techniques; D051381:Rats; D013997:Time Factors
D015220:Calcium Channels; D002116:Calcitonin; D005934:Glucagon; D004837:Epinephrine