Hypertensive vascular disease and inflammation: Mechanical and humoral mechanisms

Wr, Taylor

doi:10.1007/s11906-999-0079-5

Cited by 23 publications

(23 citation statements)

References 40 publications

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“…Increasingly it has been appreciated that evidence of an inflammatory reaction may be recorded in association with the hypertensive process (7,17,73,91,165). It is unclear whether angiotensin II, endothelin-1, or aldosterone, agents that participate in the pathophysiology of hypertension and that induce inflammation in the heart, the vasculature, and the kidney (12,82,129,171,193) or blood pressure elevation by itself, through effects on adhesion molecules, chemokines, or endothelin-1 induced by cyclic mechanical strain (18,195,201) are associated with the inflammatory response that is found in hypertension.…”

Section: Role Of Ang II In Vascular Structural Changes In Hypertensionmentioning

confidence: 99%

From bedside to bench to bedside: role of renin-angiotensin-aldosterone system in remodeling of resistance arteries in hypertension

Schiffrin

Touyz²

2004

American Journal of Physiology-Heart and Circulatory Physiology

224

159

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RESISTANCE ARTERIES are vessels of ϳ100 -300 m in lumen diameter that are an important site of resistance to blood flow. Small artery-dependent increased peripheral resistance may participate in development and complications of hypertension. The degree of remodeling of small arteries has prognostic significance over a 10-yr period, with worse prognosis for hypertensive subjects with greater remodeling. In almost all hypertensive subjects, a reduction in lumen and an increase in the media-to-lumen ratio are found, without increase in its media cross section, as a result of rearrangement of smooth muscle cells and increased collagen and fibronectin. Approximately 60% of hypertensive patients exhibit endothelial dysfunction already in stage 1 hypertension. Study of human vascular smooth muscle cells and of vessels from experimental animals has demonstrated that ANG II, aldosterone, and endothelin exert remodeling effects in large measure by activation of NADPH oxidase, and to lesser degree by stimulating xanthine oxidase and mitochondrial reactive oxygen species generation. Stimulation of angiotensin type 1 (AT 1 ) receptors (AT 1 R) leads to increased reactive oxygen species in part via activation of nonreceptor tyrosine kinases such as c-src, and of PKC and phospholipase D, and thereby contributes to endothelial dysfunction by inactivating nitric oxide (NO). Treatment of hypertensive patients with angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers, but not ␤-blockers, corrects small artery structure and endothelial dysfunction, which may favorably affect outcome in the long term, beyond the 3-5 yr of randomized clinical trials during which most antihypertensives affect outcome similarly as long as blood pressure is well controlled.

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Section: Role Of Ang II In Vascular Structural Changes In Hypertensionmentioning

confidence: 99%

From bedside to bench to bedside: role of renin-angiotensin-aldosterone system in remodeling of resistance arteries in hypertension

Schiffrin

Touyz²

2004

American Journal of Physiology-Heart and Circulatory Physiology

224

159

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“…1,2 Various types of auto-antibodies, altered number and function of T-lymphocytes, and the relationship with certain HLAgenotypes have been reported in patients with EH. 3,4 Hypertensive patients have an increased inflammatory cytokine production capacity when whole blood is stimulated ex vivo with lipopolysaccharide.…”

Section: Introductionmentioning

confidence: 99%

The −174 G/C polymorphism of the interleukin-6 gene promoter and essential hypertension in an elderly Italian population

et al. 2002

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Several studies have proposed a relationship between blood pressure and inflammation. Interleukin-6 (IL-6) is a multifunctional cytokine involved in inflammation and tissue injury and potentially influencing blood pressure. Recently, a common polymorphism of the IL-6 gene, associated with differences in the transcription rate of the protein, has been described. The aim of this study was to investigate a possible association between genetic variations of the −174GC polymorphism of the IL-6 gene promoter and hypertension in humans. IL-6 gene promoter polymorphism was evaluated by polymerase chain reaction followed by restriction enzyme analysis in 210 elderly Italian patients affected by essential

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“…The importance of ROS in vascular injury lies in the fact that their production is positively regulated by many of the cytokines whose expression is increased after injury, and also by oscillatory shear stress and mechanical disruption (Taylor 1999). Whereas low levels of ROS are necessary for normal vascular function, excess production or impaired ROS removal, in a proinflammatory environment, regulates virtually all of the cellular responses to injury, including monocyte adhesion; platelet aggregation; inflammatory gene induction; VSMC apoptosis, proliferation and migration; matrix degradation and impaired endotheliumdependent relaxation.…”

mentioning

confidence: 99%

Basic Mechanisms of Oxidative Stress and Reactive Oxygen Species in Cardiovascular Injury

Papaharalambus

Griendling

2007

Trends in Cardiovascular Medicine

290

224

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The development of vascular disease has its origins in an initial insult to the vessel wall by biological or mechanical factors. The disruption of homeostatic mechanisms leads to alteration of the original architecture of the vessel and its biological responsiveness, contributing to acute or chronic diseases such as stroke, hypertension and atherosclerosis. Endothelial dysfunction, macrophage infiltration of the vessel wall, and proliferation and migration of smooth muscle cells all involve different types of reactive oxygen species, produced by various vessel wall components. Although basic science and animal research have clearly established the role of reactive oxygen species in the progression of vascular disease, the failure of clinical trials with antioxidant compounds has underscored the need for better antioxidant therapies and a more thorough understanding of the role of reactive oxygen species in cardiovascular physiology and pathology.The fundamental processes underlying the development of vascular diseases such as atherosclerosis, restenosis and hypertensive vascular remodeling have their origins in an initial insult to the vessel wall. Such an insult may arise from mechanical disruption that occurs during percutaneous coronary angioplasty or at regions of oscillatory shear stress, or it can result from biological causes, such as hypercholesterolemia, excess free radicals, diabetes, increased concentrations of plasma homocysteine, or infectious agents. Injury promotes disruption of the homeostatic mechanisms of the endothelial protective barrier, changing its natural properties, increasing its adhesiveness to leukocytes and altering its permeability. This endothelial dysfunction also leads to the formation of vasoactive molecules, which in turn induce inflammatory genes, inactivate nitric oxide (NO • ) and its protective functions, and activate matrix metalloproteinases, leading to extracellular matrix remodeling, and increased smooth muscle cell (VSMC) growth, migration and proliferation. Each of these processes contributes to thickening of the vessel wall or the formation of lesions that can lead to hypertension, acute myocardial infarction and stroke. Reactive Oxygen Species and Vascular InjuryIn the past decade a staggering amount of evidence implicates a common denominator, reactive oxygen species (ROS), in the development of most cardiovascular diseases (Figure 1). Superoxide (O 2 •− ) and hydrogen peroxide (H 2 O 2 ) are two of the most biologically important ROS in the cardiovascular system, and are produced in vascular cells by a number of oxidases, including the NADPH oxidases (Nox) and xanthine oxidase, lipoxygenases, cytochrome p450,

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Hypertensive vascular disease and inflammation: Mechanical and humoral mechanisms

Cited by 23 publications

References 40 publications

From bedside to bench to bedside: role of renin-angiotensin-aldosterone system in remodeling of resistance arteries in hypertension

From bedside to bench to bedside: role of renin-angiotensin-aldosterone system in remodeling of resistance arteries in hypertension

The −174 G/C polymorphism of the interleukin-6 gene promoter and essential hypertension in an elderly Italian population

Basic Mechanisms of Oxidative Stress and Reactive Oxygen Species in Cardiovascular Injury

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