Summary
This study was undertaken to evaluate the physiological role, if any, of dopamine
(DA) in modulating parathyroid hormone (PTH) and calcitonin (CT) secretion in man.
Infusion of DA (5 μg/kg/min) into 6 normal men, decreased serum immunoreactive prolactin
(iPRL) and concomitantly increased serum iPTH to 140 ± 6.8% of baseline (P < 0.01)
at 30 min, wth decline thereafter, despite continuation of the DA infusion. Serum
iCT levels did not significantly change. Chlorpromazine (50 mg IM), decreased serum
iPTH to 75 ± 5.4% and 79 ± 3.7% of baseline (P < 0.01) at 30 and 60 min, respectively,
associated with an increase in iPRL. There was subsequent return of iPTH to baseline
even though iPRL remained elevated. iCT levels did not significantly change. These
observations would suggest that DA may play a physiological role in iPTH, but not
iCT, secretion. However, infusion of more nearly physiological doses of DA (0.02,
0.2, and 2.0 μg/kg/min) lowered serum iPRL to levels similar to those after the larger
DA dose, but with no concomitant increase in either iPTH or iCT. Also, 1) the DA agonist
bromocriptine decreased serum iPRL without modifying iPTH or iCT; 2) the DA precursor,
levodopa, and the DA antagonist, metoclopramide, had no effect on serum iPTH or iCT
levels. These studies suggest that 1) the transient stimulatory effect of DA on iPTH
secretion is pharmacological, and 2) DA does not have a physiological role in secretion
of iPTH or iCT in man.
Key-Words
Parathyroid hormone
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Calcitonin-Dopamine
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Dopaminergic
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Prolactin
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Secretion
