Effect of pertussis toxin on calcium influx in three contraction models.

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.