Pranidipine, a long acting 1,4-dihydropyridine calcium channel blocker, prolongs nitric oxide (NO)-mediated relaxation of rat aorta; it prolongs acetylcholine-induced relaxation in presence of endothelium as well as nitroglycerin-induced relaxation in absence of endothelium. In rat aorta the effect of pranidipine on NO-mediated relaxation is cyclic guanosine monophosphate (cGMP)-independent, but in guinea pig carotid artery the same effect of pranidipine is cGMP-dependent. It has been reported that in co-cultured human endothelial and smooth muscle cells pranidipine, at a higher concentration (10(-6) M), enhances vasorelaxant effect of NO by blocking NO decomposition. The enhancement of NO action by pranidipine differs from the direct NO-releasing action of other 1,4-dihydropyridines. It is expected that enhancement of NO-induced vasodilatation will lead to a venodilator action in vivo and less peripheral edema. The target organ protective effects of pranidipine are also reviewed in this article.

中文翻译：

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普拉尼地平是一种1,4-二氢吡啶类钙通道阻滞剂，可增强一氧化氮诱导的血管舒张作用。

长效1,4-二氢吡啶类钙通道阻滞剂普拉尼地平可延长一氧化氮（NO）介导的大鼠主动脉松弛。它在存在内皮的情况下延长了乙酰胆碱引起的舒张，而在没有内皮存在的情况下延长了硝酸甘油引起的舒张。在大鼠主动脉中，普拉尼地平对NO介导的舒张的作用是环鸟苷单磷酸（cGMP）依赖性的，但是在豚鼠的颈动脉中，普拉尼地平的相同作用也是cGMP依赖性的。据报道，在共培养的人内皮细胞和平滑肌细胞中，普拉尼地平以更高的浓度（10（-6）M）通过阻止NO分解而增强NO的血管舒张作用。普兰地平增强NO的作用不同于其他1,4-二氢吡啶的直接NO释放作用。预期NO诱导的血管扩张的增强将导致体内的血管扩张作用和较少的外周水肿。本文还综述了普拉尼平对靶器官的保护作用。