Yorio T, Henry S L, Hodges D H, Caffrey J L
Biochem Pharmacol. 1983 Mar 15;32(6):1113-8. doi: 10.1016/0006-2952(83)90634-2.
The calcium ionophore A23187 (IP) inhibited the antidiuretic hormone (ADH)-stimulated hydro-osmotic response in toad urinary bladder but had no effect on the osmotic transfer of water in the absence of hormone. Extracellular calcium was necessary for this effect at lower but not at higher IP concentrations. The hydro-osmotic response to exogenous cyclic AMP was unaltered by IP, but the same response produced by inhibition of phosphodiesterase was reduced significantly. Cyclic AMP concentrations in isolated toad bladder epithelial cells were reduced by 50% with IP or exogenous prostaglandin E2 (PGE2). Indomethacin, a prostaglandin synthesis inhibitor, prevented the inhibitory actions of the IP on the ADH-mediated response. Collectively, these observations suggest a key role for cellular calcium in modulating the actions of antidiuretic hormone and are consistent with the hypothesis that the ionophore, through increasing intracellular calcium, stimulates the synthesis of prostaglandins which have a negative feedback on adenylcyclase. This effect would terminate the action of the hormone.
钙离子载体A23187（IP）抑制了抗利尿激素（ADH）刺激的蟾蜍膀胱水渗透反应，但在无激素情况下对水的渗透转运无影响。在较低但非较高IP浓度时，细胞外钙对此效应是必需的。IP对外源性环磷酸腺苷（cAMP）的水渗透反应无改变，但抑制磷酸二酯酶产生的相同反应则显著降低。IP或外源性前列腺素E2（PGE2）可使分离的蟾蜍膀胱上皮细胞中的cAMP浓度降低50%。前列腺素合成抑制剂吲哚美辛可防止IP对ADH介导反应的抑制作用。总体而言，这些观察结果表明细胞钙在调节抗利尿激素的作用中起关键作用，并且与以下假设一致：离子载体通过增加细胞内钙来刺激前列腺素的合成，而前列腺素对腺苷酸环化酶具有负反馈作用。这种效应将终止激素的作用。
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