Gripois D, Valens M, Diarra A
J Auton Nerv Syst. 1986 Feb;15(2):165-78. doi: 10.1016/0165-1838(86)90012-3.
The adrenal medulla of normal, hypothyroid and hyperthyroid young rats was stimulated by insulin-induced hypoglycaemia. In normal rats, insulin-induced adrenal epinephrine secretion increases during the first 10 days of post-natal life. Hypothyroidism retards the development of adrenal response; hyperthyroidism facilitates the development of this response. At 14 days, when insulin-induced adrenal epinephrine depletion is the same for all groups, the recovery of adrenal catecholamines stores after depletion is linear and takes less than 48 h. Recovery rate is slightly slower for hyperthyroid rats than for either hypothyroid or control rats at 14 days. Following epinephrine depletion, adrenal tyrosine hydroxylase (TH) and dopamine-beta-hydroxylase (DBH) activities are increased for a few days in the control rats, corresponding to a transsynaptic induction. Hypothyroidism impairs TH induction and completely suppresses DBH induction; hyperthyroidism impairs TH induction, but has no effect on DBH induction. These data show that the various processes related to CA synthesis, in the adrenal medulla of the developing rat, are controlled in different ways by the thyroid hormones.
通过胰岛素诱导的低血糖刺激正常、甲状腺功能减退和甲状腺功能亢进的幼鼠肾上腺髓质。在正常大鼠中，胰岛素诱导的肾上腺肾上腺素分泌在出生后的前10天增加。甲状腺功能减退会延缓肾上腺反应的发育；甲状腺功能亢进则促进这种反应的发育。在14天时，当所有组胰岛素诱导的肾上腺肾上腺素耗竭相同时，耗竭后肾上腺儿茶酚胺储存的恢复呈线性，且耗时不到48小时。在14天时，甲状腺功能亢进大鼠的恢复速度比甲状腺功能减退大鼠或对照大鼠略慢。肾上腺素耗竭后，对照大鼠的肾上腺酪氨酸羟化酶（TH）和多巴胺-β-羟化酶（DBH）活性会在几天内增加，这与跨突触诱导相对应。甲状腺功能减退会损害TH诱导并完全抑制DBH诱导；甲状腺功能亢进会损害TH诱导，但对DBH诱导没有影响。这些数据表明，发育中大鼠肾上腺髓质中与儿茶酚胺合成相关的各种过程受到甲状腺激素的不同控制。
