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本文介绍用膜片箝方法研究腺苷抑制蛙垂体中叶促黑素细胞激素（αＭＳＨ）分泌的分子电生理机制．研究结果表明，腺苷激活Ａ１型受体后，通过４条途径减少αＭＳＨ分泌所需要的钙内流：１）激活电压不敏感的钾电导引起的膜电位超级化；２）增高延缓外向整流的钾电导引起动作电位时间缩短；３）瞬时失活外向钾电流增加引起的细胞兴奋性降低；４）抑制Ｌ和Ｎ型钙电流的内流．白日咳毒素敏感的Ｇ蛋白参与腺苷对离子通道的调节作用，究竟是通过直接的偶联还是经过细胞内第二信使的传递尚需进一步证明．我们的结果已排除腺苷酸环化酶系统的途径
This paper introduces the use of patch-clamp method to study the molecular electrophysiological mechanism of adenosine inhibition frog pituitary melanocyte stimulating hormone (α MSH) secretion. The results show that adenosine activates the A1 receptor, through four ways to reduce the α-MSH secretion required calcium influx: 1) activation of voltage-sensitive potassium-induced membrane potential hyper-sensitivity; 2) increased delayed outbound Rectified potassium conductance leads to shortened action potentials; 3) Decreased cell excitability due to transient inactivation of outward potassium currents; and 4) Inhibition of influx of L and N type calcium currents. Pertussis toxin-sensitive G protein involved in adenosine on the ion channel regulation, whether through direct coupling or through the second messenger within the cell still needs further evidence. Our results have excluded the adenylate cyclase system pathway