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Effects of the Calcium Channel Activator BAY-K-8644 on in Vitro Secretion of Calcitonin and Parathyroid Hormone^*

CARY W. COOPER, SUSAN A. BOROSKY, PATRICK E. FARRELL and ODD S. STEINSLAND

Department of Pharmacology and Toxicology, University of Texas Medical Branch Galveston, Texas 77550

Abstract

The recently discovered calcium (Ca) channel activator BAY-K-8644 [methyl-l,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)pyridine-5-carboxylate], an analog of the calcium channel blockers nifedipine and nitrendipine, was tested to determine its potential for altering hormone secretion in an in vitro system designed to study concurrent secretion of calcitonin (CT) and PTH. Addition of BAY-K-8644 (10^–4-10^–6 M) to medium (1 mM Ca) bathing baby rat thyroparathyroids enhanced secretion of CT at least 2- to 4-fold and suppressed PTH release by as much as 75–85%. Addition of BAYK-8644 alone to medium containing high (2.5 mM) Ca did not further enhance the already high rate of CT release, nor did it cause any further suppression of PTH secretion. BAY-K-8644 did not stimulate CT release or suppress PTH release in the absence of medium Ca. Addition of the Ca channel blocker nitrendipine (10^–6 M) inhibited CT release at either 1 or 2.5 mM Ca, and at 1 mM Ca, nitrendipine negated the simulatory effect of 10^–5 M BAY-K-8644 on CT release. However, at 2.5 mM Ca, 10^–6 M BAY-K-8644 reversed the marked inhibitory effect of 10^–5 M nitrendipine on CT release. At 1 mM Ca, PTH secretion was inhibited equally well by BAY-K-8644 and nitrendipine, and both agents together caused a further suppression of PTH release. The results indicate that Ca entry into the thyroid Ccell and parathyroid chief cell may occur via classical voltagesensitive Ca channels and that the newly described Ca channel activator BAY-K-8644 should prove useful as a probe for studying hormone secretion in Ca-dependent secretory systems. (Endocrinology 118: 545–549, 1986)

Footnotes

^* This work was supported in part by USPHS Program Project AM-35608 and Grant AM-32060 from the NIADDK. Portions of this work were presented in abstract form at the 67th Meeting of The Endocrine Society, Baltimore, MD, June 19, 1985, p 97.

To whom all correspondence and requests for reprints should be addressed.

Received July 17, 1985.

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