SRIF-sensitive compartmentalization of stored rGH is abolished by hypothyroidism.

Rat adenohypophyses lose immuno- and bioassayable growth hormone in hypothyroidism. We examined whether the somatotroph also loses mechanisms for intracellular hormone compartmentalization during hypothyroidism. A series of identical perifusions was performed using pituitary tissue from thyroidectomized rats before and after thyroxine replacement. Somatostatin (SRIF), (Bu)2cAMP and potassium ion were employed to produce a wide range of hormone release responses. Growth hormone synthesis diminished with hypothyroidism and increased with thyroid hormone replacement. Growth hormone release was therefore expressed as a percent of pituitary content to circumvent effects of variable content. Post-somatostatin rebound release was lost in hypothyroidism: it fell progressively after thyroidectomy (day 7 = 45% of control; day 14 = 11%; day 71 = 3%) and was restored by thyroxine replacement (day 2 = 24%; day 5 = 50%; day 9 = 102%). In conclusion, hypothyroid somatotrophs lose the ability to sequester stored hormone in a SRIF-sensitive compartment. Thyroxine replacement restores that capability. Thus, SRIF-sensitive rGH compartmentalization is thyroid hormone dependent.