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目的研究佛波脂(phorbol 12-myristate 13-acetate,PMA)及microcys-tine-LR(MCYST-LR)对卒中易感型自发性高血压大鼠(SHRsp)及常压对照Wistar大鼠肠系膜动脉A4-A5段分支阻力血管平滑肌电压依赖性钙通道的影响。方法采用膜片箝全细胞钡电流方式记录钙通道的活动。结果佛波脂激活蛋白激酶C(PKC)或MCYST-LR抑制细胞蛋白磷酸酶(PPⅠA、PPⅡA)而相对增加磷酸化过程,均可激活内脏阻力血管平滑肌电压依赖性钙通道。结论 PMA的激活效应,在SHRsp,是使开放的L型钙通道活动显著增强,T型钙通道活动略有增加;而在Wistar大鼠,则以T型钙电流增加为主。MCYST-LR仅使SHRsp的L型钙通道活动显著增强。提示在分析高血压的外周阻力增高机制时,应进一步分析PKC和磷酸化机制对钙通道各电流成分的影响。
Objective To investigate the effects of phorbol 12-myristate 13-acetate (PMA) and microcys-tine-LR (MCYST-LR) on stroke-prone spontaneously hypertensive rats (SHRsp) and normal pressure Wistar rats Effect of voltage-dependent calcium channel resistance in vascular smooth muscle of A4-A5 limbs. Methods Patch clamp whole-cell barium current was used to record calcium channel activity. Results Phospholipid-activated calcium kinase C (PKC) or MCYST-LR inhibited cell protein phosphatase (PPⅠA, PPⅡA) and increased the phosphorylation of visceral resistance vascular smooth muscle voltage-dependent calcium channel. Conclusions The activating effect of PMA in SHRsp is to increase the activity of open L-type calcium channel and increase the activity of T-type calcium channel. In Wistar rats, the increase of T-type calcium current is the main factor. MCYST-LR significantly increased L-type calcium channel activity in SHRsp only. It is suggested that in the analysis of the mechanism of peripheral resistance increase in hypertension, we should further analyze the influence of PKC and phosphorylation mechanism on the current components of calcium channel.