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lüll Pranidipine, a 1,4-dihydropyridine calcium channel blocker that enhances nitric oxide-induced vascular relaxation Mori T; Takase H; Toide K; Hirano T; Kambe T; Nakayama N; Schwartz ACardiovasc Drug Rev 2001[Spr]; 19 (1): 1-8Pranidipine, 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.|Amlodipine/pharmacology[MESH]|Animals[MESH]|Calcium Channel Blockers/*pharmacology[MESH]|Cyclic GMP/metabolism[MESH]|Dihydropyridines/*pharmacology[MESH]|Drug Synergism[MESH]|Endothelium, Vascular/drug effects/metabolism[MESH]|Humans[MESH]|Muscle, Smooth, Vascular/drug effects/physiopathology[MESH]|Myocardial Contraction/drug effects/physiology[MESH]|Nitric Oxide/*pharmacology[MESH]|Vasodilation/*drug effects/physiology[MESH]|Vasodilator Agents/*pharmacology[MESH] |