Watanabe J, Keitoku M, Hangai K, Karibe A, Takishima T
First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Am J Physiol. 1993 Feb;264(2 Pt 2):H547-52. doi: 10.1152/ajpheart.1993.264.2.H547.
We tested the hypothesis that protein kinase C (PKC) activation plays a major role in alpha-adrenergic augmentation of the myogenic response in rat isolated arterioles. Lumen diameter measured was with a video-monitored microscopic system. Lumen diameter did not change (131 +/- 5 vs. 126 +/- 6 microns) despite an increase in lumen pressure from 40 to 100 mmHg. Phenylephrine (Phe; 3 x 10(-7) M) augmented the myogenic response, since lumen diameter decreased significantly from 117 +/- 8 to 101 +/- 8 microns. High potassium (40 mM) failed to augment the myogenic response, while constricting the vessels to nearly the same extent as did Phe. PKC inhibitors 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine dihydrochloride (H-7, 5 x 10(-5) M, n = 7) and staurosporine (3 x 10(-9) M, n = 7) abolished the Phe-induced augmentation. H-7 and staurosporine depressed the myogenic response even without Phe. PKC activators phorbol 12,13-dibutyrate (3 x 10(-9) M; n = 7) and 4 beta-phorbol 12-myristate 13-acetate (6 x 10(-8) M; n = 6) constricted the vessels by 11 +/- 2 and 18 +/- 3%, respectively. However, PKC activators failed to augment the myogenic response. These results suggest that PKC activation does not play a major role in alpha-adrenergic augmentation of the myogenic response in rat skeletal arterioles.
蛋白激酶C（PKC）激活在大鼠离体小动脉肌源性反应的α-肾上腺素能增强中起主要作用。通过视频监测显微镜系统测量管腔直径。尽管管腔压力从40 mmHg增加到100 mmHg，但管腔直径并未改变（131±5微米对126±6微米）。去氧肾上腺素（Phe；3×10⁻⁷ M）增强了肌源性反应，因为管腔直径从117±8微米显著减小至101±8微米。高钾（40 mM）未能增强肌源性反应，同时使血管收缩至与Phe几乎相同的程度。PKC抑制剂1-（5-异喹啉磺酰基）-2-甲基哌嗪二盐酸盐（H-7，5×10⁻⁵ M，n = 7）和星形孢菌素（3×10⁻⁹ M，n = 7）消除了Phe诱导的增强作用。即使没有Phe，H-7和星形孢菌素也会抑制肌源性反应。PKC激活剂佛波醇12,13-二丁酸酯（3×10⁻⁹ M；n = 7）和4β-佛波醇12-肉豆蔻酸酯13-乙酸酯（6×10⁻⁸ M；n = 6）分别使血管收缩11±2%和18±3%。然而，PKC激活剂未能增强肌源性反应。这些结果表明，PKC激活在大鼠骨骼肌小动脉肌源性反应的α-肾上腺素能增强中不起主要作用。
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