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Endocrinology, Vol 127, 711-715, Copyright © 1990 by Endocrine Society

ARTICLES

Differences in the actions of calcium versus lanthanum to influence parathyroid hormone release

LA Fitzpatrick
University of Texas Health Science Center, San Antonio.

PTH release from bovine parathyroid cells is inhibited by increasing concentrations of extracellular calcium (Ca2+). We have proposed that this inhibition is mediated by Ca2+ channels via a G-protein. To further test this hypothesis, we evaluated the effect of lanthanum (La3+), a potent Ca2+ channel antagonist that does not cross the cell membrane. PTH release was determined in dispersed bovine parathyroid cells by radioimmunoassay: extracellular Ca2+ concentration was 0.2 mM. PTH release was inhibited by maximal concentrations of La3+ to a greater extent than by Ca2+: 93% inhibition by La3+ vs. 40% by Ca2+. La3+ was more potent (set-point = 0.12 mM) than Ca2+ (set-point = 1.2 mM). Incubation of parathyroid cells with pertussis toxin, which inactivates a G-protein(s) and blocks inhibition by Ca2+, did not block the inhibition of PTH release by La3+ at the concentrations tested. The Ca2+ ionophore A23187, which potentiates the effect of Ca2+, did not enhance the inhibition of PTH release by La3+. Increasing concentrations of calcium enhanced the inhibition of PTH release by the Ca2+ channel agonist, (+)202-791. The Ca2+ channel antagonist, (-)202- 791, shifted the Ca2+ inhibition curve to the right. La3+ did not alter the inhibition of PTH release by the Ca2+ channel agonist but blocked the stimulatory effect of the Ca2+ channel antagonist, (-)202-791. In summary: 1) La3+, which blocks Ca2+ channels and does not cross cell membranes, effects a greater inhibition of PTH release than Ca2+; 2) La3+, like Ca2+, overrides the effect of Ca2+ channel antagonist (-)202- 791; and 3) La3+, unlike Ca2+, inhibits PTH release by a mechanism that is independent of a pertussis toxin-sensitive G-protein. There may be two cell surface sites that recognize La3+ and Ca2+ independently.




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Copyright © 1990 by The Endocrine Society