The role of calcium in the induction of refractoriness to cyclic AMP stimulation by TSH.

The role of calcium in the induction of refractoriness to cyclic AMP stimulation by TSH.
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钙在诱导 TSH 对环 AMP 刺激不应性中的作用。

DOI:
10.1016/0026-0495(85)90158-1
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发表时间:
1985
期刊:
Metabolism: clinical and experimental
影响因子:
--
通讯作者:
Field,JB
Field,JB
中科院分区:
--
文献类型:
--
作者:
Chayoth,R;Arem,R;Yoshimura,Y;Field,JB

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牛甲状腺切片初始暴露于25 mU/mL促甲状腺激素(TSH)2小时后,诱导环磷酸腺苷(AMP)产生的刺激减少,随后再加入TSH,但不改变前列腺素E1(PGE 1)的作用。甲状腺切片在含或不含2 mmol/L乙二醇双(β-氨乙基醚)-N,N′ =四乙酸(EGTA)的无钙缓冲液中孵育,可阻止TSH和PGE 1诱导的对TSH和PGE 1刺激的脱敏,尽管随后孵育中存在钙。TSH诱导的脱敏没有修改增加钙浓度高达50 mmol/L在初始孵育。然而,TSH对cAMP水平的刺激作用随着第一次孵育中钙浓度的增加而降低。在至少1 mmol/L钙的存在下,20 μmol/L离子载体A-23187与甲状腺切片的初始孵育降低了在随后孵育期间首次加入25 mU/mL TSH对环AMP的刺激。在这些条件下,A-23187对PGE 1刺激cAMP没有影响。这些结果表明,钙可能发挥作用,TSH诱导的,但不是PGE 1,脱敏环AMP的形成。
An initial exposure of beef thyroid slices to 25 mU/mL thyroid-stimulating hormone (TSH) for two hours induces a diminished stimulation of cyclic adenosine monophosphate (AMP) production upon subsequent readdition of TSH but does not modify the effect of prostaglandin E1(PGE1. Incubation of thyroid slices in calcium-free buffer with or without 2 mmol/L ethylene glycol bis (β-aminoethyl ether)—N,N′ = tetracetic acid (EGTA) prevented desensitization induced by TSH and PGE1, to the subsequent stimulation by TSH and PGE1, respectively, despite the presence of calcium in subsequent incubations. TSH-induced desensitization was not modified by increasing the calcium concentration up to 50 mmol/L in the initial incubation. However, the stimulatory effect of TSH upon cyclic AMP levels was decreased as the calcium concentration in the first incubation was increased. In the presence of at least 1 mmol/L calcium, an initial incubation of thyroid slices with 20 μmol/L ionophore A-23187 decreased the stimulation of cyclic AMP by 25 mU/mL TSH added to the slices for the first time during a subsequent incubation. Under these conditions, A-23187 had no effect on PGE1stimulation of cyclic AMP. These results indicate that calcium may play a role in the TSH-induced, but not PGE1, desensitization of cyclic AMP formation.
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DOI: --
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