Regulation of hormone secretion and cytosolic Ca2+ by extracellular Ca2+ in parathyroid cells and C-cells: role of voltage-sensitive Ca2+ channels.
Regulation of hormone secretion and cytosolic Ca2+ by extracellular Ca2+ in parathyroid cells and C-cells: role of voltage-sensitive Ca2+ channels.
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甲状旁腺细胞和 C 细胞中细胞外 Ca2+ 对激素分泌和胞质 Ca2+ 的调节：电压敏感 Ca2+ 通道的作用。
DOI：
10.1016/0003-9861(88)90378-5
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发表时间：
1988
影响因子：
3.9
通讯作者：
Fischer,JA
中科院分区：
文献类型：
--
作者：
Muff,R;Nemeth,EF;Haller-Brem,S;Fischer,JA
在分散的牛甲状旁腺细胞和大鼠甲状腺髓样癌（rMTC）细胞系中，检测了分别作为电压敏感性Ca 2+通道激动剂和拮抗剂的两种二氢吡啶对映体（+）202-791和（−）202-791对细胞溶质Ca 2+浓度（[Ca 2 +]i）和激素分泌的影响。在这两种细胞类型中，细胞外Ca 2+浓度的小幅增加诱发了短暂的[Ca 2 +]i持续增加，如用Fura-2测量的。细胞外Ca ~（2+）升高，[Ca ~（2+）] i增加，刺激rMTC细胞分泌降钙素（CT）和降钙素基因相关肽（CGRP），但抑制甲状旁腺激素（PTH）的分泌。Ca 2+通道激动剂（+）202-791刺激而拮抗剂（-）202-791抑制rMTC细胞中细胞外Ca 2+诱导的[Ca 2 +] i的瞬时和持续增加。（+）202-791和（-）202-791分别相应地增强和抑制CT和CGRP的分泌。相反，无论是激动剂还是拮抗剂都不影响甲状旁腺细胞[Ca ~（2+）] i和PTH分泌。去极化浓度的细胞外K+增加rMTC细胞[Ca 2 +] i和激素分泌，这两种反应被加强或抑制的Ca 2+通道激动剂或拮抗剂，分别。结果表明，电压敏感的Ca 2+内流的调节胞浆Ca 2+和激素分泌的rMTC细胞中的主要作用。另一方面，甲状旁腺细胞似乎缺乏电压敏感的Ca 2+内流途径，并通过一些替代机制调节PTH分泌。
The two dihydropyridine enantiomers, (+)202-791 and (−)202-791, that act as voltage-sensitive Ca2+channel agonist and antagonist, respectively, were examined for effects on cytosolic Ca2+concentrations ([Ca2+]i) and on hormone secretion in dispersed bovine parathyroid cells and a rat medullary thyroid carcinoma (rMTC) cell line. In both cell types, small increases in the concentration of extracellular Ca2+evoked transient followed by sustained increases in [Ca2+]i, as measured with fura-2. Increases in [Ca2+]iobtained by raised extracellular Ca2+were associated with a stimulation of secretion of calcitonin (CT) and calcitonin gene-related peptide (CGRP) in rMTC cells, but an inhibition of secretion of parathyroid hormone (PTH) in parathyroid cells. The Ca2+channel agonist (+)202-791 stimulated whereas the antagonist (−)202-791 inhibited both transient and sustained increases in [Ca2+]iinduced by extracellular Ca2+in rMTC cells. Secretion of CT and CGRP was correspondingly enhanced and depressed by (+)202-791 and (−)202-791, respectively. In contrast, neither the agonist nor the antagonist affected [Ca2+]iand PTH secretion in parathyroid cells. Depolarizing concentrations of extracellular K+increased [Ca2+]iand hormone secretion in rMTC cells and both these responses were potentiated or inhibited by the Ca2+channel agonist or antagonist, respectively. The results suggest a major role of voltage-sensitive Ca2+influx in the regulation of cytosolic Ca2+and hormone secretion in rMTC cells. Parathyroid cells, on the other hand, appear to lack voltage-sensitive Ca2+influx pathways and regulate PTH secretion by some alternative mechanism.