Effect of magnesium on parathyroid cells: evidence for two sensing receptors or two intracellular pathways?
H. Miki, P. B. Maercklein and L. A. Fitzpatrick Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota, USA. It currently remains controversial as to the intracellular mechanisms coupled to the inhibition of parathyroid hormone (PTH) secretion that are modulated by extracellular divalent...
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Veröffentlicht in: | American journal of physiology: endocrinology and metabolism 1997-01, Vol.272 (1), p.E1-E6 |
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Zusammenfassung: | H. Miki, P. B. Maercklein and L. A. Fitzpatrick
Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota, USA.
It currently remains controversial as to the intracellular mechanisms
coupled to the inhibition of parathyroid hormone (PTH) secretion that are
modulated by extracellular divalent cations. To study mechanisms
responsible for regulation of PTH release by cations, we investigated the
effect of Mg2+ on cytosolic Ca2+ levels ([Ca2+]i) and PTH secretion in
single isolated bovine parathyroid cells. Addition of 9.0 mM Mg2+ evoked a
spike of [Ca2+]i in approximately 80% of cells in the presence of
extracellular Ca2+. Mg2+ decreased steady-state [Ca2+]i, which represented
inhibition of influx of extracellular Ca2+ in 13-78% of cells. The
percentage of cells that had a decline in steady-state [Ca2+]i after
exposure to Mg2+ was dependent on the extracellular Ca2+ concentration. The
effect of Mg2+ on intracellular Ca2+ response was dose dependent.
Extracellular Mg2+ inhibited PTH secretion in cells that showed decline in
steady-state [Ca2+]i, although cells that showed a spike after addition of
Mg2+ secreted more PTH than cells that did not show a spike. The spike of
[Ca2+]i and decline in steady-state [Ca2+]i that occur in response to
extracellular Mg2+ may be caused independently by two distinct mechanisms
that differentially regulate secretion of PTH. |
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ISSN: | 0193-1849 0002-9513 1522-1555 |
DOI: | 10.1152/ajpendo.1997.272.1.e1 |