Abstract
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.
Original language | English (US) |
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Pages (from-to) | 37-45 |
Number of pages | 9 |
Journal | Molecular and Cellular Endocrinology |
Volume | 44 |
Issue number | 1 |
DOIs | |
State | Published - Jan 1986 |
Keywords
- immunoprecipitation
- perifusion in vitro
- rat pituitary
- somatotroph
ASJC Scopus subject areas
- Biochemistry
- Molecular Biology
- Endocrinology