Hove K, Sand O
Acta Physiol Scand. 1981 Sep;113(1):37-43. doi: 10.1111/j.1748-1716.1981.tb06858.x.
The acute effects of various drugs on the release of parathyroid hormone (PTH) in goats were studied by local infusions in vivo. Infusions of Ca2+ or Sr2+ reduced the PTH secretion rate, whereas hypocalcemia induced by EDTA increased the PTH release. Blockers of voltage sensitive Ca2+ channels (verapamil, D-600 and nifedipine) lowered the PTH secretion rate, while infusion of 4-aminopyridine, which is a blocker of voltage sensitive K+ channels, increased the PTH release. These effects were not due to altered beta-adrenergic tonus, since the effects persisted when the drugs were administered during continuous infusion of the beta-blocker propranolol. We suggest that the parathyroid cells possess voltage sensitive K+ and Ca2+ channels, and that exocytosis of stored PTH depends on the influx of extracellular Ca2+ as in other secretory cells. In order to explain the inverse relationship between the plasma Ca2+ level and the PTH release, we postulate a suppressive effect of the plasma Ca2+ on the membrane permeability to Ca2+ in parathyroid cells.
通过体内局部输注的方法，研究了多种药物对山羊甲状旁腺激素（PTH）释放的急性影响。输注Ca2+或Sr2+可降低PTH分泌率，而由乙二胺四乙酸（EDTA）诱导的低钙血症则增加PTH释放。电压敏感性Ca2+通道阻滞剂（维拉帕米、D - 600和硝苯地平）降低PTH分泌率，而输注电压敏感性K+通道阻滞剂4 - 氨基吡啶则增加PTH释放。这些效应并非由于β - 肾上腺素能张力改变所致，因为在持续输注β - 阻滞剂普萘洛尔期间给予这些药物时，效应仍然存在。我们认为甲状旁腺细胞具有电压敏感性K+和Ca2+通道，并且储存的PTH的胞吐作用与其他分泌细胞一样，依赖于细胞外Ca2+的内流。为了解释血浆Ca2+水平与PTH释放之间的负相关关系，我们推测血浆Ca2+对甲状旁腺细胞膜对Ca2+的通透性具有抑制作用。
