Den Hertog A, Nelemans A, Van den Akker J
Department of Pharmacology and Clinical Pharmacology, University of Groningen, The Netherlands.
Eur J Pharmacol. 1988 Jul 14;151(3):357-63. doi: 10.1016/0014-2999(88)90531-6.
The action of bradykinin on the smooth muscle of guinea-pig taenia caeci was studied by measuring changes in membrane potential, the contractile state of the muscle cells and intracellular calcium concentrations at 22 degrees C in the presence of tetrodotoxin, yohimbine, prazosin, propranolol and atropine. The bradykinin response was characterised by an initial hyperpolarization and suppression of spike activity followed by a sustained depolarization and an increased spike activity accompanied by inhibition of the phasic contractions, an increase in muscle tone and the development of phasic contractions, respectively. The actions of bradykinin were not affected after B1-bradykinin receptors were blocked with des-Arg9-[Leu8]bradykinin. The events induced by bradykinin were accompanied by an increase in the intracellular calcium concentration, as monitored by quin-2 fluorescence. The hyperpolarization and depolarization persisted in the presence of diltiazem (10(-5) M) and in calcium-free conditions. The hyperpolarization could be evoked only once in the absence of calcium and was inhibited in the presence of apamin and after stimulation of alpha 1-adrenoceptors or P2-purinoceptors. Membrane conductance was decreased during the sustained depolarization. The membrane depolarization was abolished after the sodium concentration gradient was reduced. These results show a multiple action of bradykinin mediated via B2-receptors: (1) on calcium mobilization associated with activation of potassium channels; (2) on calcium release from intracellular stores and (3) on receptor-activated sodium channels.
在22摄氏度下，于存在河豚毒素、育亨宾、哌唑嗪、普萘洛尔和阿托品的条件下，通过测量膜电位变化、肌肉细胞收缩状态和细胞内钙浓度，研究了缓激肽对豚鼠盲肠带平滑肌的作用。缓激肽反应的特征为：先是初始超极化和动作电位活动受抑制，随后是持续去极化和动作电位活动增加，分别伴有相位性收缩受抑制、肌张力增加和相位性收缩的出现。用去-精氨酸9-[亮氨酸8]缓激肽阻断B1-缓激肽受体后，缓激肽的作用不受影响。缓激肽诱导的这些事件伴随着细胞内钙浓度的增加，这是通过喹啉-2荧光监测的。在存在地尔硫䓬（10^(-5) M）和无钙条件下，超极化和去极化持续存在。在无钙情况下，超极化只能诱发一次，并且在存在蜂毒明肽时以及在刺激α1-肾上腺素能受体或P2-嘌呤能受体后受到抑制。在持续去极化期间，膜电导降低。在钠浓度梯度降低后，膜去极化消失。这些结果表明缓激肽通过B2-受体介导多种作用：（1）对与钾通道激活相关的钙动员；（2）对细胞内钙库的钙释放；（3）对受体激活的钠通道。
