KCl과 phenylephrine에 의한 대동맥 수축에서 Ca2+ 길항제와 protein kinase 억제제들의 비교 효과

Comparative Effects of Ca2+ Antagonists and Protein Kinase Unhibitors on Rat Aorta Contraction Induced by KCl and Phenylephrine

To investigate the difference of contractile mechanism between KCl and phenylephrine-induced contraction, we observed effects of Ca2+ antagonists and protein kinase inhibitors on aorta contraction of rats. Verapamil dose-dependently inhibited the contraction induced by KCl and pheylephrine, the inhibitory effect of verapamil was more potent in KCl-induced contraction than phenylephrine-induced contraction. Econazole and TMB-8 significantly inhibited KCl-induced contraction but did not inhibit phenylephrine-induced contraction. Staurosporine dose-dependently inhibited both KCl and phenylephrine-induced contraction. Genistein and calmodulin antagonists (W-7 and trifluoperazine) also inhibited both contraction in a dose dependent manner. However, the inhibitory effects of genistein and calmodulin antagonists were more potent in pheylephrine-induced contraction than KCl-induced contraction. These results suggest that involvements of Ca2+ channel and protein kinase in rat aorta contraction were dependent on agonist causing aort smooth muscle contraction.