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Departments of Anatomy and Medicine and the Biologic Resources Laboratory, University of Illinois at the Medical Center, and Veterans Administration West Side Medical Center Chicago, Illinois 60612; Department of Obstetrics and Gynecology, University of Iowa Hospitals and Clinics Iowa City, Iowa 52242
Address all correspondence and requests for reprints to: Roy M.Pitkin, M.D., Department of Obstetrics and Gynecology, University of Iowa Hospitals and Clinics, Iowa City, Iowa 52242.
The calcitonin (CT) response to provocative stimuli in the near-term fetus was assessed in 15 pregnant rhesus monkeys. Using a preparation permitting infusion and sequential sampling of fetal blood with the fetus in utero and the amniotic sac intact, calcium (20 mg/kg), glucagon (50 µg), or saline was infused into 5 fetuses over 2 h and sampling was continued for an additional 2 h. Plasma samples were analyzed for total calcium (Ca) and immunoreactive CT. In zero time samples, the fetuses were significantly hypercalcemic (4.81 ± 0.11 vs. 3.79 ± 0.09 meq/liter; P < 0.001) and hypercalcitonemic (307 ± 22 vs. 263 ± 15 pg/ml; P < 0.05) relative to their mothers. Calcium infusion sufficient to increase the fetal plasma Ca level by 57–64% provoked an increase in fetal CT values of 44–50%; both Ca and CT levels returned to pretreatment levels with cessation of the calcemic stimulus. Glucagon also evoked a statistically significant fetal CT response of 23–29%, which, in turn, was associated with a hypocalcemic effect. In contrast to the fetal responses observed with calcium and glucagon, Ca and CT values in the mother did not change significantly. No maternal or fetal alterations in CT resulted from control (saline) infusions. These results indicate that the monkey fetus is capable of responding appropriately to calcemic and glucagon stimuli by releasing CT in a manner similar to that previously observed in the adult.
* This work was supported by grants from the NICHHD (HD-09373), The National Foundation-March of Dimes (6-141), and the Medical Research Program of the V.A.
Received February 19, 1980.
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