Abstract
Dihydropyridine-based calcium antagonists (DHPs) are widely used drugs for the treatment of hypertension and angina pectoris. We, along with others, have recently found that nifedipine, one of the most widely used DHPs, inhibits apoptotic cell death of endothelial cells (ECs) as well as vascular inflammation and subsequently improves endothelial function in patients with cardiovascular risk factors, including hypertension and/or diabetes, thus slowing the development and progression of atherosclerosis in these patients. Several papers have suggested that nifedipine exerts beneficial metabolic effects in vivo through its anti-inflammatory properties as well. However, the underlying molecular mechanisms for the cardiometabolic actions of nifedipine remain to be elucidated, because ECs do not possess voltage-operated L-type calcium channels. Meanwhile, we have very recently found that Bay w 9798, a dihydropyridine structurally related to nifedipine with no calcium antagonistic ability, has anti-oxidative and anti-inflammatory properties in vitro. In this paper, we review the role of oxidative stress in the development of vascular injury, especially focusing on the relationships between advanced glycation end products-receptor system, oxidized low-density lipoprotein and tumor necrosis factor-α and vasculopathy. We further discuss the potential clinical utility of anti-oxidative properties of nifedipine on various cardiometabolic disorders.
Keywords: Advanced glycation end products, diabetic vascular complications, insulin resistance, nitric oxide, oxidative stress
Current Medicinal Chemistry
Title: Role of Oxidative Stress in the Development of Vascular Injury and its Therapeutic Intervention by Nifedipine
Volume: 15 Issue: 2
Author(s): Sho-ichi Yamagishi, Kazuo Nakamura and Takanori Matsui
Affiliation:
Keywords: Advanced glycation end products, diabetic vascular complications, insulin resistance, nitric oxide, oxidative stress
Abstract: Dihydropyridine-based calcium antagonists (DHPs) are widely used drugs for the treatment of hypertension and angina pectoris. We, along with others, have recently found that nifedipine, one of the most widely used DHPs, inhibits apoptotic cell death of endothelial cells (ECs) as well as vascular inflammation and subsequently improves endothelial function in patients with cardiovascular risk factors, including hypertension and/or diabetes, thus slowing the development and progression of atherosclerosis in these patients. Several papers have suggested that nifedipine exerts beneficial metabolic effects in vivo through its anti-inflammatory properties as well. However, the underlying molecular mechanisms for the cardiometabolic actions of nifedipine remain to be elucidated, because ECs do not possess voltage-operated L-type calcium channels. Meanwhile, we have very recently found that Bay w 9798, a dihydropyridine structurally related to nifedipine with no calcium antagonistic ability, has anti-oxidative and anti-inflammatory properties in vitro. In this paper, we review the role of oxidative stress in the development of vascular injury, especially focusing on the relationships between advanced glycation end products-receptor system, oxidized low-density lipoprotein and tumor necrosis factor-α and vasculopathy. We further discuss the potential clinical utility of anti-oxidative properties of nifedipine on various cardiometabolic disorders.
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Cite this article as:
Yamagishi Sho-ichi, Nakamura Kazuo and Matsui Takanori, Role of Oxidative Stress in the Development of Vascular Injury and its Therapeutic Intervention by Nifedipine, Current Medicinal Chemistry 2008; 15 (2) . https://dx.doi.org/10.2174/092986708783330557
DOI https://dx.doi.org/10.2174/092986708783330557 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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