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本文探讨了α1a，α1b，α1d三种亚型肾上腺素受体（AR）激动时细胞内Ca2＋浓度（[Ca2＋]i）升高的信号转导途径。在稳定表达三亚型α1－AR的HEK293细胞系中，用fura－2方法描记细胞内Ca2＋信号强弱的变化。结果显示，百日咳毒素（PTX）对去甲肾上腺素激动三亚型α1－AR而引起的[Ca2＋]i升高无影响，U-73122和PMA明显抑制[Ca2＋]i升高；CalphoshtinC和PWA过夜预处理可翻转PMA的抑制作用；Forskolin和Rp-cAMPs对α1-AR介导的[Ca2＋]；升高无影响，但Quercetin和Tyrphostin可抑制[Ca2＋]；升高峰值，对平台期幅值则无影响。因此，在HEK293细胞，三亚型α1－AR可通过PTX非敏感G蛋白激活PLG而介导磷酸肌醇-Ca2＋信号系统，PKC磷酸化系统既抑制α1－AR介导的细胞内贮存Ca2＋释放，又抑制细胞外Ca2＋内流；cAMP系统不参与α1－AR介导Ca2＋信号的调节，酪氨酸激酶可能参与这一过程。
This article explored the signal transduction pathways of elevated intracellular Ca2 + concentration ([Ca2 +] i) during the activation of adrenergic receptors (ARs) in α1a, α1b and α1d subtypes. In the HEK293 cell line stably expressing the Sialotype α1-AR, the change of intracellular Ca2 + signal intensity was characterized by the fura-2 method. The results showed that pertussis toxin (PTX) had no effect on the increase of [Ca2 +] i induced by norepinephrine-stimulated Sanya α1-AR, and U-73122 and PMA significantly inhibited the increase of [Ca2 +] i; Calphoshtin C and PWA overnight Forskolin and Rp-cAMPs had no effect on α1-AR-mediated increase of [Ca2 +]; however, Quercetin and Tyrphostin inhibited [Ca2 +]; the peak value was increased and the plateau amplitude was not influences. Thus, in HEK293 cells, the Sial-type α1-AR mediates phosphoinositide-Ca2 + signaling through the activation of PLG by the PTX-insensitive G protein. The PKC phosphorylation system inhibits α1-AR-mediated intracellular Ca2 + release, Inhibition of extracellular Ca2 + influx; cAMP system is not involved in α1-AR-mediated Ca2 + signal regulation, tyrosine kinases may be involved in this process.