Marcus R, Orner F B
Endocrinology. 1977 Nov;101(5):1570-8. doi: 10.1210/endo-101-5-1570.
We studied the cAMP response of cultured rat calvaria to parathyroid hormone (PTH) and prostaglandins (PG) in order to test the hypothesis that PTH action is mediated by PG. PTH and PGE1 each caused an 8-fold increase in tissue cAMP during 15 min incubation. There was an additive response to the combination of the two agonists at maximally effective individual concentrations. Similar results were obtained when adenylate cyclase activity in bone homogenates were measured. Calvaria incubated for 60 min with PGE1 were desensitized to further stimulation by PGE1, but responded normally to PTH. Indomethacin, aspirin and phenylbutazone, 10(-5)M, had no effect on the cAMP response to PTH. At millimolar concentration these agents did block the hormone response; however, the response to exogenous PGE1 and the fluoride-sensitive adenylate cyclase were also inhibited. Thus, it appears that the effects of high concentrations of the anti-inflammatory drugs on cAMP formation are non-specific. Our results suggest that receptors in bone for PTH and prostaglandins are separate and independent, and that the cAMP response to PTH is not mediated by prostaglandins.
我们研究了培养的大鼠颅骨对甲状旁腺激素（PTH）和前列腺素（PG）的环磷酸腺苷（cAMP）反应，以检验PTH作用由PG介导这一假说。在15分钟的孵育过程中，PTH和PGE1各自使组织cAMP增加了8倍。在最大有效个体浓度下，两种激动剂联合使用有相加反应。测量骨匀浆中的腺苷酸环化酶活性时也得到了类似结果。用PGE1孵育60分钟的颅骨对PGE1的进一步刺激产生脱敏，但对PTH反应正常。10(-5)M的吲哚美辛、阿司匹林和保泰松对cAMP对PTH的反应无影响。在毫摩尔浓度下，这些药物确实阻断了激素反应；然而，对外源性PGE1的反应以及对氟敏感的腺苷酸环化酶也受到抑制。因此，看来高浓度抗炎药对cAMP形成的作用是非特异性的。我们的结果表明，骨中PTH和前列腺素的受体是分开且独立的，并且对PTH的cAMP反应不是由前列腺素介导的。
