Grześk Elżbieta, Tejza Barbara, Wiciński Michał, Malinowski Bartosz, Szadujkis-Szadurska Katarzyna, Baran Lilianna, Kowal Elżbieta, Grześk Grzegorz
Department of Pediatrics, Hematology and Oncology, Collegium Medicum, Nicolaus Copernicus University, Bydgoszcz 85094, Poland.
Department of Pharmacology and Therapeutics, Collegium Medicum, Nicolaus Copernicus University, Bydgoszcz 85094, Poland.
Biomed Rep. 2014 Jul;2(4):584-588. doi: 10.3892/br.2014.274. Epub 2014 May 12.
Pertussis toxin (PTX) blocks G protein activation and inhibits signal transmission from the activated receptor to effectors that are specific for the G protein-coupled receptor. The aim of the present study was to evaluate the effect of PTX on vascular smooth muscle cells that were stimulated pharmacologically with phenylephrine (α-adrenoceptor agonist), mastoparan-7 (direct G-protein activator) and Bay K8644 (direct calcium channel activator). The changes in perfusion pressure that were proportional to the degree of phenylephrine-induced constriction of rat tail arteries were assessed. Concentration-response curves (CRCs) that were obtained for phenylephrine, mastoparan-7 and Bay K8644 presented a sigmoidal association. A significantly reduced calcium influx to the cytoplasm in the presence of mastoparan-7 resulted in a significant rightward shift of the CRCs with a significant reduction in maximal responses. The presence of PTX did not change mastoparan-7 and Bay K8644-induced contraction, whereas the significant inhibition of phenylephrine-induced contraction was found. The results of the experiments indicated that PTX significantly inhibited phenylephrine-induced contraction of vascular smooth muscle cells by inhibition of calcium influx from the intra- and extracellular calcium space. PTX did not change the smooth muscle contraction that was induced by mastoparan-7 and Bay K8644. The predominant effect of mastoparan-7 may be associated with other binding sites as compared to the G-protein or PTX may bind to other sites than mastoparan-7.
百日咳毒素（PTX）可阻断G蛋白激活，并抑制从激活的受体到G蛋白偶联受体特异性效应器的信号传递。本研究的目的是评估PTX对用去氧肾上腺素（α-肾上腺素能受体激动剂）、马斯托帕兰-7（直接G蛋白激活剂）和Bay K8644（直接钙通道激活剂）进行药理学刺激的血管平滑肌细胞的影响。评估了与去氧肾上腺素诱导的大鼠尾动脉收缩程度成比例的灌注压变化。去氧肾上腺素、马斯托帕兰-7和Bay K8644获得的浓度-反应曲线（CRC）呈现出S形关系。在存在马斯托帕兰-7的情况下，细胞质中钙内流显著减少，导致CRC显著右移，最大反应显著降低。PTX的存在并未改变马斯托帕兰-7和Bay K8644诱导的收缩，而发现去氧肾上腺素诱导的收缩受到显著抑制。实验结果表明，PTX通过抑制细胞内和细胞外钙空间的钙内流，显著抑制去氧肾上腺素诱导的血管平滑肌细胞收缩。PTX并未改变马斯托帕兰-7和Bay K8644诱导的平滑肌收缩。与G蛋白相比，马斯托帕兰-7的主要作用可能与其他结合位点有关，或者PTX可能与马斯托帕兰-7以外的其他位点结合。
