Gardner D G, Brown E M, Aurbach G D
Metabolism. 1983 Apr;32(4):355-8. doi: 10.1016/0026-0495(83)90043-4.
Ouabain, at concentrations of 3 X 10(-4)-10(-3) M, inhibited secretion of PTH approximately 50% in a freshly dispersed bovine parathyroid cell preparation. This inhibition was found with both unstimulated and secretagogue-stimulated PTH release. Reductions in PTH secretion were found at all concentrations of Ca++ tested between 0.3 mM and 2.0 mM and in the presence of the divalent cation chelators EDTA and EGTA, indicating that extracellular Ca++ is not an absolute requirement for the inhibition. The ouabain inhibition did not appear to be mediated through changes in either adenylate cyclase activity or total cellular cAMP, implying a locus distal to the generation of this cyclic nucleotide. The data suggest that transmembrane potential and/or distribution of monovalent cations across the plasma membrane is important in the maintenance of PTH secretion. The mechanisms involved in this control do not appear to involve extracellular Ca++ directly.
哇巴因在浓度为3×10⁻⁴ - 10⁻³ M时,可使新鲜分离的牛甲状旁腺细胞制剂中甲状旁腺激素(PTH)的分泌抑制约50%。这种抑制在未刺激和促分泌剂刺激的PTH释放中均有发现。在0.3 mM至2.0 mM之间测试的所有Ca²⁺浓度以及存在二价阳离子螯合剂乙二胺四乙酸(EDTA)和乙二醇双乙醚二胺四乙酸(EGTA)的情况下,均发现PTH分泌减少,这表明细胞外Ca²⁺并非这种抑制的绝对必要条件。哇巴因的抑制作用似乎不是通过腺苷酸环化酶活性或细胞内总环磷酸腺苷(cAMP)的变化介导的,这意味着其作用位点在这种环核苷酸生成的下游。数据表明跨膜电位和/或单价阳离子在质膜上的分布对维持PTH分泌很重要。这种控制所涉及的机制似乎并不直接涉及细胞外Ca²⁺。