Dihydropyridine‐ and voltage‐sensitive Ca 2+ entry in human parathyroid cells

Patch‐clamp and fluorescence measurements of cytoplasmic Ca 2+ concentration ([Ca 2+ ] i ) were performed to directly detect extracellular Ca 2+ entry into cultured parathyroid cells from patients with secondary hyperparathyroidism. Cells loaded with fluo‐3 AM or fluo‐4 AM showed a transient increase in fluorescence (Ca 2+ transient) following 10 s exposure to 150 m m K + solution in the presence of millimolar concentrations of external Ca 2+ . The Ca 2+ transient was completely inactivated after 30–40 s exposure to the high‐K + solution, was reduced by dihydropyridine antagonists and was enhanced by FPL‐64176, an L‐type Ca 2+ channel agonist. The electrophysiological and pharmacological properties of the whole‐cell Ca 2+ and Ba 2+ currents were similar to those of L‐type Ca 2+ channels. The Ca 2+ transients induced by 10 s exposure to 3.0 m m extracellular Ca 2+ concentration ([Ca 2+ ] o ) were inhibited by dihydropyridine antagonists and were partly inactivated following 30–40 s exposure to the high‐K + solution. These results demonstrate, for the first time, that human parathyroid cells express L‐type‐like Ca 2+ channels that are possibly involved in the [Ca 2+ ] o ‐induced change in [Ca 2+ ] i . This Ca 2+ entry system might provide a compensatory pathway for the negative feedback regulation of parathyroid hormone secretion, especially in hyperplastic conditions in which the Ca 2+ ‐sensing receptor is poorly expressed.