Endocrinology, Vol 108, 1690-1696, Copyright © 1981 by Endocrine Society

ARTICLES

Evidence for a possible role for Ca++ in the 3,5,3'-triiodothyronine inhibition of thyrotropin-releasing hormone-induced secretion of thyrotropin by rat anterior pituitary in vitro

MP Schrey and PR Larsen

The present study was undertaken to determine whether T3 could modify anterior pituitary Ca++ metabolism under basal conditions and in the presence of TRH. Paired hemipituitaries from hypothyroid rats were preincubated with T3 (10(-7) M) for 2 h, allowed to accumulate 45Ca++ for the third hour, and repeatedly washed in static incubations or superfused for the next 2 h with isotope-free medium and finally with TRH (10(-8) M) for 10 min. T3 treatment had no effect on the basal pattern of isotope loss throughout the 2-h wash period. TRH stimulated 45Ca++ fractional efflux from a basal value of 0.76 +/- 0.10% to 1.66 +/- 0.38% min-1 (P less than 0.02; mean +/- SD; n = 9). T3 reduced TRH- stimulated efflux to 1.30 +/- 0.20% min-1, while basal values were unaltered (0.70 +/- 0.10% min-1). Similarly, T3 inhibited the TSH response to TRH from 480% to 200% of basal secretion. T3 pretreatment also inhibited the basal uptake of 45Ca++ when a La+++ displacement protocol was employed from 1751 +/- 36 to 1400 +/- 61 cpm/mg pituitary (mean +/- SEM; n = 13; P less than 0.001). Similar data for 45Ca++ efflux were obtained in experiments where tissue was superfused. rT3 did not affect basal or stimulated 45Ca++ efflux, and inhibition of stimulated secretion and 45Ca++ efflux by T3 was dependent on preincubation. The data indicate that T3 is capable of altering anterior pituitary Ca++ homeostasis. Such a mechanism could be involved in the T3-induced inhibition of TRH-stimulated TSH release which appears to require a redistribution of cellular Ca++.