Alterations in the Vasoreactivity of Hypertensive Rat Aortic Rings: Role of Nitric Oxide and Superoxide Radicals

Hegde, Laxminarayan G.; Srivastava, Pallavi; Kumari, Ranjana; Dikshit, Madhu

doi:10.3109/10641969809053253

Cited by 24 publications

(15 citation statements)

References 31 publications

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“…Amounts of antioxidant scavengers, such as SOD, glutathione peroxidase, catalase, and vitamin C and E, are decreased in atherosclerotic patients, including patients with PAD [83]. NADH/NADPH oxidase is a major source of production of ROS in vessel walls [84]. It has also been shown that ascorbic acid restores impaired endothelium-dependent vasodilation in patients with essential hypertension [10], hypercholesterolemia [11,12], and CAD [13,14].…”

Section: Oxidative Stress By Cell Therapy and Gene Therapymentioning

confidence: 97%

Oxidative Stress, Endothelial Function and Angiogenesis Induced by Cell Therapy and Gene Therapy

Higashi¹,

Nishioka²,

Umemura³

et al. 2006

CPB

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Recently, clinical studies have shown that novel therapies, including cell implantation and transfer of gene encoding for angiogenic growth factors, are effective in patients with critical limb ischemia who have no other treatment option. This concept is called therapeutic angiogenesis. Cell therapy involves implantation of bone-marrow or peripheral mononuclear cells and endothelial progenitor cells (CD34(+) cells) in the gastrocnemius of the ischemic leg. Gene therapy involves delivery of vascular endothelial growth factor and fibroblast growth factor using a plasmid or adenoviral vector. Critical limb ischemia is associated with endothelial dysfunction as well as excess oxidative stress. A balance of oxidative stress and nitric oxide play an important role in the development of atherosclerosis in patients with peripheral arterial diseases. It has been reported that both cell therapy and gene therapy improve endothelial function in the resistant artery of an ischemic limb. Cell therapy or gene therapy in combination with pharmacological therapy as an antioxidant could be useful for restoration of endothelial function and prevention of development of atherosclerosis in patients with critical limb ischemia. In this review, we discuss the relationships between oxidative stress, endothelial function, and angiogenesis and the mechanism by which therapeutic angiogenesis improves endothelial function.

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Section: Oxidative Stress By Cell Therapy and Gene Therapymentioning

confidence: 97%

Oxidative Stress, Endothelial Function and Angiogenesis Induced by Cell Therapy and Gene Therapy

Higashi¹,

Nishioka²,

Umemura³

et al. 2006

CPB

View full text Add to dashboard Cite

show abstract

“…Amounts of antioxidant scavengers, such as SOD, glutathione peroxidase (GPx), catalase, and vitamin C and E, are decreased in atherosclerotic patients, including patients with hypertension and hypercholesterolemia [121]. NADH/NADPH oxidase, which is a major source of production of ROS in vessel walls, is activated in hypertensive rats [122,123]. It has also been shown that ascorbic acid (vitamin C) restores impaired endotheliumdependent vasodilation in patients with essential hypertension [8], hypercholesterolemia [16,124], and CAD [20,125].…”

Section: -2 Decrease In No Inactivation: Restoration Of Oxidative Smentioning

confidence: 99%

Angiotensin II Type I Receptor Blocker and Endothelial Function in Humans: Role of Nitric Oxide and Oxidative Stress

Higashi

Chayama²,

Yoshizumi

2005

CMCCHA

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Recent large clinical trials have shown that angiotensin II type I receptor blockers (ARBs) reduce cardiovascular morbidity and mortality in patients with heart failure, acute myocardial infarction, and hypertension. However, the mechanism underlying antiatherogenic effects of ARBs remains unclear. The vascular endothelium is involved in the release of various vasodilators, including nitric oxide (NO), prostacyclin, and endothelium-derived hyperpolarizing factor as well as vasoconstrictors. NO plays an important role in the regulation of vascular tone, the inhibition of platelet aggregation, and the suppression of smooth muscle cell proliferation. Several investigators have reported impairment in endothelium-dependent vasodilation in the forearm, coronary, and renal vasculature in cardiovascular diseases, including hypertensive patients. Cardiovascular diseases are associated with alteration in endothelial function. Endothelial dysfunction is the initial step in the pathogenesis of atherosclerosis. Anti-renin-angiotensin system agents, angiotensin-converting enzyme (ACE) inhibitors improve endothelial function in patients with hypertension, diabetes mellitus, and coronary artery disease. It is well known that ACE inhibitors augment endothelium-dependent vasodilation through an increase in NO bioavailability, by an increase in NO production and a decrease in NO inactivation. ARBs are also thought to prevent cardiovascular complications through an augmentation of endothelial function. In this review, we focus on recent findings and putative mechanisms of the beneficial effects of ARBs on endothelial function.

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“…60 NADPH oxidase, which is a major source of production of ROS in vessel walls, is activated in hypertensive rats. 61,62 It has also been shown that ascorbic acid restores impaired endothelium-dependent vasodilation in patients with essential hypertension. 63 Therefore, enhanced production of ROS and an attenuated antioxidant system may contribute to endothelial dysfunction in patients with hypertension.…”

Section: Endothelial Dysfunction and Hypertensionmentioning

confidence: 99%

Endothelial dysfunction and hypertension in aging

2012

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Hypertension is one of the common diseases in the elderly. The prevalence of hypertension markedly increases with advancing age. Both aging and hypertension have a critical role in cardiovascular and cerebrovascular complications. Although aging and hypertension, either independently or collectively, impair endothelial function, aging and hypertension may have similar cascades for the pathogenesis and development of endothelial dysfunction. Nitric oxide (NO) has an important role in regulation of vascular tone. Decrease in NO bioavailability by endothelial dysfunction would lead to elevation of blood pressure. An imbalance of reduced production of NO or increased production of reactive oxygen species, mainly superoxide, may promote endothelial dysfunction. One possible mechanism by which the prevalence of hypertension is increased in relation to aging may be advancing endothelial dysfunction associated with aging through an increase in oxidative stress. In addition, endothelial cell senescence is also involved in aging-related endothelial dysfunction. In this review, we focus on recent findings and interactions between endothelial function, oxidative stress and hypertension in aging.

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Alterations in the Vasoreactivity of Hypertensive Rat Aortic Rings: Role of Nitric Oxide and Superoxide Radicals

Abstract: Attenuation in the Ach induced NO release and augmentation in the superoxide radical generation seems to play an important role in the modulation of vasoreactivity following renal hypertension in rats.

Cited by 24 publications

References 31 publications

Oxidative Stress, Endothelial Function and Angiogenesis Induced by Cell Therapy and Gene Therapy

Oxidative Stress, Endothelial Function and Angiogenesis Induced by Cell Therapy and Gene Therapy

Angiotensin II Type I Receptor Blocker and Endothelial Function in Humans: Role of Nitric Oxide and Oxidative Stress

Endothelial dysfunction and hypertension in aging

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