What question did this study set out to answer?

Determine the potency and specificity of dihydropyridine calcium antagonists in blocking depolarization-dependent hormone release and calcium influx in normal and transformed pituitary cells.

May 1, 1985AJP Cell Physiology

Dihydropyridine Ca2+ antagonists: potent inhibitors of secretion from normal and transformed pituitary cells

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Authors

JEJohn J. EnyeartThe Ohio State University Wexner Medical Center TAToru AizawaMukogawa Women's University PHPatricia M. HinkleUniversity of Rochester Medical Center

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Implication

In vitro study shows dihydropyridines potently inhibit depolarization-dependent secretion in pituitary cells, indicating functional similarity to smooth muscle calcium channels.

Key Points

Determine the potency and specificity of dihydropyridine calcium antagonists in blocking depolarization-dependent hormone release and calcium influx in normal and transformed pituitary cells.
Assessed potassium chloride (KCl)-stimulated and thyrotropin-releasing hormone-stimulated prolactin secretion in GH4C1 pituitary cells and normal rat pituitary cells.
Evaluated the inhibitory potency of dihydropyridines (nimodipine, nisoldipine, nifedipine) compared with other organic calcium antagonists (verapamil, cinnarizine, diltiazem) across KCl concentrations from 18.8 to 53.8 mM.
Measured depolarization-dependent 45Ca2+ uptake in GH4C1 cells treated with antagonist compounds.
Nimodipine, nisoldipine, and nifedipine potently and reversibly inhibited KCl-stimulated prolactin secretion from GH4C1 cells with estimated IC50 values of 1.8 nM, 1.8 nM, and 6.0 nM, respectively.
Non-dihydropyridine antagonists verapamil, cinnarizine, and diltiazem required much higher concentrations to inhibit prolactin secretion from GH4C1 cells, displaying estimated IC50 values of 1,000 nM, 1,100 nM, and 3,500 nM, respectively.
Dihydropyridines and verapamil suppressed depolarization-stimulated prolactin secretion in normal pituitary cells at identical concentrations to GH4C1 cells and similarly blocked KCl-stimulated 45Ca2+ uptake.

Cite This Study

Enyeart et al. (1985) studied this question.

synapsesocial.com/papers/6a71b37bac440176ef2a4bfc https://doi.org/10.1152/ajpcell.1985.248.5.c510

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Implication

In vitro study shows dihydropyridines potently inhibit depolarization-dependent secretion in pituitary cells, indicating functional similarity to smooth muscle calcium channels.

Dihydropyridine Ca2+ antagonists: potent inhibitors of secretion from normal and transformed pituitary cells

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Implication

Key Points

Cite This Study

Dihydropyridine Ca2+ antagonists: potent inhibitors of secretion from normal and transformed pituitary cells

Discussion

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Implication

Key Points

Cite This Study

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