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薬理と治療
Abstract
Objective Cilnidipine an L╱N type calcium channel blocker, has been reported to reduce serum lipid peroxide level in patients with essential hypertension. However, the mechanism remains to be incompletely understood. In this study, we examined the effects of cilnidipine on hydrogen peroxide(H2O2)release from human polymorphonuclear leukocyte. Methods Polymorphonuclear leukocytes, isolated from healthy volunteers or patients with essential hypertension, were stimulated with phorbol 12︱myristate 13︱acetate(PMA)to measure H2O2 release using a scopoletin method, which was assessed in the presence or absence of each dihydropyridine calcium channel blockers;cilnidipine, amlodipine, nifedipine, nilvadipine and nitrendipine. Results Cilnidipine inhibited PMA︱stimulated H2O2 release from polymorphonuclear leukocytes isolated from healthy volunteers in a concentration︱dependent manner(IC50=0.91μM). Amlodipine also inhibited H2O2 release(IC50=6.06μM), whose potency was weaker than that of cilnidipine. On the other hand, nifedipine, nilvadipine and nitrendipine failed to inhibit the H2O2 release(IC50>10μM). Furthermore, cilnidipine inhibited PMA︱stimulated H2O2 release from polymorphonuclear leukocytes in patients with essential hypertension. Conclusions Cilnidipine inhibited PMA︱stimulated H2O2 release from human polymorphonuclear leukocytes more potently than other calcium channel blockers in this study. These findings suggest that cilnidipine may have beneficial effects on cardiovascular complications in patients with essential hypertension through the antioxidative effects by inhibition of reactive oxygen species release.
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