Gill J, DeSouza V, Wakeling A, Dandona P, Jeremy J Y
Department of Chemical Pathology and Human Metabolism, Royal Free Hospital and School of Medicine, London, England.
J Clin Endocrinol Metab. 1992 Feb;74(2):441-6. doi: 10.1210/jcem.74.2.1346146.
[45Ca2+] Uptake was studied in response to adrenaline, isoprenaline, noradrenaline, and (Bu)2cAMP in platelets from patients with anorexia nervosa. In both controls and anorectics, adrenaline, isoprenaline, noradrenaline, and (Bu)2cAMP stimulated [45Ca2+] uptake. In receptor subtype characterisation studies on control platelets, adrenaline-stimulated [45Ca2+] uptake was blocked by yohimbine (an alpha 2-adrenoceptor antagonist) and the specific beta 2-adrenoceptor antagonist ICI 118,551, but not by atenolol (a beta 1-antagonist). Isoprenaline action was blocked by ICI 118,551, but not by yohimbine. Noradrenaline-stimulated [45Ca2+] uptake was blocked by yohimbine but not by ICI 118,551. In platelets from anorectic patients, there was a significant increase in noradrenaline-stimulated [45Ca2+] uptake, a significant diminution in adrenaline and isoprenaline-stimulated [45Ca2+] uptake, but no significant difference in (Bu)2cAMP-stimulated [45Ca2+] uptake, when compared with controls. Basal uptake was also significantly enhanced in anorectics and was found to be inhibited with verapamil but not adrenoceptor antagonist. These data firstly indicate that both alpha 2- and beta 2-adrenoceptor activation elicits [45Ca2+] uptake by platelets. It is proposed that this stimulated [45Ca2+] uptake does not reflect changes in cytosolic Ca2+ but to localized changes of Ca2+ at the plasma membrane, possibly associated with receptor activation, per se. The respective increase and decrease of alpha- and beta-adrenoceptor activity in platelets from anorectic patients is in accord with other reports of changes of adrenoceptor number and type in platelets and other cells from anorectic patients. There may also be an increase in calcium channel activity in platelets from anorectics.
对神经性厌食症患者血小板中[45Ca2+]摄取情况进行了研究，观察其对肾上腺素、异丙肾上腺素、去甲肾上腺素和双丁酰环磷腺苷（(Bu)2cAMP）的反应。在对照组和神经性厌食症患者中，肾上腺素、异丙肾上腺素、去甲肾上腺素和(Bu)2cAMP均能刺激[45Ca2+]摄取。在对对照血小板进行的受体亚型特征研究中，育亨宾（一种α2 -肾上腺素能受体拮抗剂）和特异性β2 -肾上腺素能受体拮抗剂ICI 118,551可阻断肾上腺素刺激的[45Ca2+]摄取，但阿替洛尔（一种β1 -拮抗剂）则不能。异丙肾上腺素的作用可被ICI 118,551阻断，但不能被育亨宾阻断。去甲肾上腺素刺激的[45Ca2+]摄取可被育亨宾阻断，但不能被ICI 118,551阻断。与对照组相比，神经性厌食症患者血小板中，去甲肾上腺素刺激的[45Ca2+]摄取显著增加，肾上腺素和异丙肾上腺素刺激的[45Ca2+]摄取显著减少，但(Bu)2cAMP刺激的[45Ca2+]摄取无显著差异。神经性厌食症患者的基础摄取也显著增强，且发现可被维拉帕米抑制，但不能被肾上腺素能受体拮抗剂抑制。这些数据首先表明，α2 -和β2 -肾上腺素能受体激活均能引发血小板摄取[45Ca2+]。有人提出，这种刺激的[45Ca2+]摄取并不反映胞质Ca2+的变化，而是反映质膜上Ca2+的局部变化，可能与受体激活本身有关。神经性厌食症患者血小板中α -和β -肾上腺素能受体活性的相应增加和减少，与其他关于神经性厌食症患者血小板和其他细胞中肾上腺素能受体数量和类型变化的报道一致。神经性厌食症患者血小板中的钙通道活性可能也有所增加。
