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JournalISSN: 1573-4021

Current Hypertension Reviews 

Bentham Science Publishers
About: Current Hypertension Reviews is an academic journal published by Bentham Science Publishers. The journal publishes majorly in the area(s): Blood pressure & Angiotensin II. It has an ISSN identifier of 1573-4021. Over the lifetime, 418 publications have been published receiving 4531 citations.


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Journal ArticleDOI
TL;DR: The aim of this review is to present a novel focus on the role of oxidative stress in the pathophysiology of hypertension and recent biomarkers which are found to be associated with reactive oxygen species and therole of antioxidants as therapy of hypertension.
Abstract: Free radicals or reactive oxygen species (ROS) are generated by oxygen metabolism which is balanced by the rate of oxidant formation and the rate of oxidant elimination. Oxidative stress is a result of imbalance between the generation of reactive oxygen species (ROS) and the antioxidant defence systems. Hypertension is one of the major risk factors for cardiovascular diseases and is considered as a leading cause of mortality and morbidity. These diseases affect more than 600 million people and it has been estimated that 29% of the world population will be suffering from hypertension by 2025. It has been indicated by experimental evidence that reactive oxygen species (ROS) play an important role in the pathophysiology of hypertension. The vasculature is a rich source of NADPH oxidase which produces most of the reactive oxygen species and plays an important role in renal dysfunction and vascular damage. Recent studies indicate that increased oxidative stress is the important mediator of endothelial injury in the pathology of hypertension associated to increased production of pro oxidants such as superoxideanion hydrogen peroxide, reduced nitric oxide synthesis and decreased bioavailability of antioxidants. Oxidative stress is found to be associated with endothelial dysfunction, inflammation, hypertrophy, apoptosis, cell migration, fibrosis, and angiogenesis in relation to vascular remodelling of hypertension. Results in humans are still less conclusive inspite of data available that involve oxidative stress as a causative factor of essential hypertension. The aim of this review is to present a novel focus on the role of oxidative stress in the pathophysiology of hypertension and recent biomarkers which are found to be associated with reactive oxygen species and the role of antioxidants as therapy of hypertension.

249 citations

Journal ArticleDOI
TL;DR: Brachial-ankle pulse wave velocity (baPWV) is a unique measure of systemic arterial stiffness that is measured by brachial and tibial arterial wave analyses and the hypothesis that baPWVs-guided therapy could improve prognosis in high-risk patients is examined.
Abstract: Arterial stiffness is a vascular measure that has been reported to predict cardiovascular events. It is important to measure arterial stiffness in order to determine current vascular status and treatment strategy. Brachial-ankle pulse wave velocity (baPWV) is a unique measure of systemic arterial stiffness that is measured by brachial and tibial arterial wave analyses. Measurement of baPWV is easy and is reproducible. For more than a decade, this measure has been used broadly in East Asian countries. Meta-analysis of cohort studies conducted in the general population with hypertension, diabetes, or end-stage renal disease, and other high-risk individuals have shown that a 1 m/s increase in baPWV is associated with 12% increase in the risk of cardiovascular events. Thus, the Japanese Circulation Society has proposed that a baPWV of 1800 cm/s is a threshold for high-risk category. For baPWV to be clinically applicable, we must confirm that circulation of the lower limbs are normal by examining brachial ankle blood pressure index. In cases of peripheral arterial disease, the reliability of baPWV measurement is attenuated. To further confirm the clinical usefulness of this measure, we need to examine the hypothesis that baPWV-guided therapy could improve prognosis in high-risk patients.

156 citations

Journal ArticleDOI
TL;DR: This review focuses on the relationship between intracellular ROS formation and ED in endothelial cells or blood vessels exposed to TNF-α to provide insight into the role of this important cytokine in cardiovascular disease.
Abstract: Endothelial cell injury and dysfunction are the major triggers of pathophysiological processes leading to cardiovascular disease. Endothelial dysfunction (ED) has been implicated in atherosclerosis, hypertension, coronary artery disease, vascular complications of diabetes, chronic renal failure, insulin resistance and hypercholesterolemia. Although now recognized as a class of physiological second messengers, reactive oxygen species (ROS) are important mediators in cellular injury, specifically, as a factor in endothelial cell damage. Uncontrolled ROS production and/or decreased antioxidant activity results in a deleterious state referred to as 'oxidative stress'. A candidate factor in causing ROS production in endothelial cells is tumor necrosis factor alpha (TNF-α), a pleiotropic inflammatory cytokine. TNF-α has been shown to both be secreted by endothelial cells and to induce intracellular ROS formation. These observations provide a potential mechanism by which TNF-α may activate and injure endothelial cells resulting in ED. In this review, we focus on the relationship between intracellular ROS formation and ED in endothelial cells or blood vessels exposed to TNF-α to provide insight into the role of this important cytokine in cardiovascular disease.

138 citations

Journal ArticleDOI
TL;DR: Six mechanisms have been suggested explaining HHcy-induced endothelial dysfunction and the goal of this review is to elaborate these mechanisms and to discuss biological and molecular events related to HHCy-induced ED.
Abstract: Hyperhomocysteinemia (HHcy) is a significant and independent risk factor for cardiovascular diseases. Endothelial dysfunction (ED) is the earliest indicator of atherosclerosis and vascular diseases. We and others have shown that HHcy induced ED in human and in animal models of HHcy induced by either high-methionine load or genetic deficiency. Six mechanisms have been suggested explaining HHcy-induced ED. These include 1) nitric oxide inhibition, 2) prostanoids regulation, 3) endothelium-derived hyperpolarizing factors suppression, 4) angiotensin II receptor-1 activation, 5) endothelin-1 induction, and 6) oxidative stress. The goal of this review is to elaborate these mechanisms and to discuss biological and molecular events related to HHcy-induced ED.

105 citations

Journal ArticleDOI
TL;DR: If central and peripheral pressure calibrations are equivalent, two major methods to estimate CBP—those based on generalized pressure transfer function or radial late systolic pressure—may be comparable in their accuracy of CBP parameter estimation.
Abstract: Central aortic blood pressure (CBP) is increasingly considered a better cardiovascular prognostic marker than conventional cuff brachial blood pressure. Because CBP cannot be directly measured noninvasively, it has to be estimated from peripheral pressure pulses. To assess estimated CBP appropriately, the accuracy and features of the estimation method should be considered. The aim of this review is to provide basic knowledge and information useful for interpreting and assessing estimated CBP from a methodological point of view. Precise peripheral pressure pulse recording has been enabled by the introduction of arterial applanation tonometry, for which the radial artery may be the optimal site. An automated tonometry device utilizing a sensor array is preferable in terms of reproducibility and objectivity. Calibration of a peripheral pressure waveform has unresolved problems for any estimation method, due to imperfect brachial sphygmomanometry. However, if central and peripheral pressure calibrations are equivalent, two major methods to estimate CBP—those based on generalized pressure transfer function or radial late systolic pressure—may be comparable in their accuracy of CBP parameter estimation.

78 citations

Performance
Metrics
No. of papers from the Journal in previous years
YearPapers
202310
202217
202122
202023
201923
201818