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在酶新鲜分离的犬肠系膜上动脉平滑肌细胞，蛋白激酶Ｃ（ＰＫＣ）的激活剂佛波二丁酯（ＰＤＢ）引起的胞内Ｃａ２＋增高作用可被ＰＫＣ抑制剂１－（５－异喹啉磺酰）－２－甲基哌嗪（Ｈ７）所阻断，而哌唑嗪和普萘洛尔则不能阻断ＰＤＢ的这一作用；１０μｍｏｌ·Ｌ－１苯福林引起的胞内Ｃａ２＋增高作用可被１０和２０μｍｏｌ·Ｌ－１Ｈ７部分阻断；在无Ｃａ２＋液，Ｈ７可部分抑制苯福林引起的内Ｃａ２＋释放和外Ｃａ２＋内流，两者分别被抑制了３３±３％和５８±６％；ＫＣｌ（２０－１００ｍｍｏｌ·Ｌ－１）可浓度依赖性地引起胞内钙升高，这一作用可被１０和２０μｍｏｌ·Ｌ－１Ｈ７不同程度地阻断；ＰＤＢ引起的胞内Ｃａ２＋增高也可分别被１．２５和２．５μｍｏｌ·Ｌ－１维拉帕米部分和全部阻断。上述结果提示ＰＫＣ参与苯福林引起的部分内Ｃａ２＋释放和外Ｃａ２＋内流，但以参与外Ｃａ２＋内流为主；这一作用可能与ＰＫＣ激活，引起电压依赖性Ｃａ２＋通道开放有关。
In isolated canine isolated rat canine mesenteric artery smooth muscle cells, protein kinase C (PKC) activator of phorbol dibutyl ester (PDB) -induced intracellular Ca2 + role of PKC inhibitor 1- (5-isoquinolinesol Acyl) -2-methylpiperazine (H7), while prazosin and propranolol failed to block this effect of PDB. Elevated intracellular Ca2 + induced by 10 μmol·L-1 phenylephrine Can be partially blocked by 10 and 20μmol·L-1H7; in the absence of Ca2 + solution, H7 can partially inhibit phenylephrine-induced Ca2 + and Ca2 + influx, both of which were inhibited by 33 ± 3% and 58 ± 6 %; KCl (20-100mmol · L-1) can cause intracellular calcium concentration-dependent increase, this effect can be blocked by 10 and 20μmol·L-1H7 to varying degrees; PDB-induced increase in intracellular Ca2 + Can be partially and totally blocked by 1.25 and 2.5 μmol·L -1 verapamil respectively. The above results suggest that PKC participates in phenylephrine-induced partial Ca2 + release and extracellular Ca2 + influx, but mainly participates in extracellular Ca2 + influx. This effect may be related to the activation of PKC and the opening of voltage-dependent Ca2 + channels.