Abstract
The role of prolactin (PRL) in calcitonin (CT) release by the thyroid C cell in male rats was studied. Anterior pituitary (AP)-grafted male rats were characterized by hyperprolactinemia. Brain cortex (CX)-grafted male rats were used as control animals. AP- and CX-grafted rats were infused intravenously with CaCl2 and bled from the jugular catheter at 0, 30, 60, and 120 minutes following the CaCl2 challenge. Rat thyroid gland was incubated with or without 3-isobutyl-1-methylxanthine (IBMX) at 37 degrees C for 30 minutes. Thyroid C cells were incubated in culture medium at 37 degrees C for 60 minutes. Cyclic adenosine 3',5'-monophosphate (cAMP) in rat thyroid tissues following incubation with IBMX was extracted by 65% ethanol. AP-grafted rats had higher plasma levels of PRL and CT compared with CX-grafted rats. Both the release of CT and accumulation of cAMP in thyroid glands were higher in AP-grafted versus CX-grafted rats. Direct administration of ovine PRL (oPRL) on the thyroid glands did not increase CT secretion in vitro. Thyroid C cells of AP-grafted rats secreted more CT compared with CX-grafted rat cells. These results suggest that hyperprolactinemia increases the release of CT by thyroid C cells in rats through a cAMP-dependent pathway caused by an indirect effect of PRL.
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