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See article by Batova et al. [12] (pages 478–485) in this issue. The antihypertensive drug amlodipine (Norvasc®) is a long-acting, third-generation Ca2+ channel blocker that has been shown to limit the progression of atherosclerosis and to decrease the incidence of cardiovascular events in humans [1]. It is generally well tolerated and often used in combination with diuretics, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor antagonists and statins [2–4]. Amlodipine exhibits nanomolar affinity to dihydropyridine as well as benzothiazepine and phenylalkylamine binding sites of voltage-dependent L-type Ca2+ channels [5]. It is several-fold more lipophilic than the first- and second-generation Ca2+ channel blockers and adopts a well-defined position in the bilayer membrane [6]. It has been suggested that partitioning of amlodipine to membranes results in beneficial modification of the structure of cholesterol-rich membranes of vascular smooth muscle cells, an effect that might contribute to atheroprotection [7].Besides the well-documented inhibition of L-type Ca2+ channels, amlodipine exerts additional effects that contribute to the improvement of vascular function in hypertension and ischemic heart disease [8]. There is both in vitro and in vivo evidence indicating that dihydropyridines including amlodipine act as antioxidants preventing the progression of atherosclerosis by interfering with lipid peroxidation. However, amlodipine has pharmacological properties distinct from other Ca2+ channel blockers. Probably most relevant to the antihypertensive and antiplatelet effects of the drug is the release of endothelium-derived nitric oxide (NO). …

Translocation of endothelial nitric oxide synthase: Another feat of amlodipine, a cardiovascular jack-of-all-trades