Is Vascular Endothelial Growth Factor a Missing Link Between Hypertension and Inflammation?

Morishita, Ryuichi

doi:10.1161/01.hyp.0000138689.29876.b3

Cited by 14 publications

(10 citation statements)

References 15 publications

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“…It is believed that subjects with hypertension tend to develop chronic, low-grade systemic inflammation38–40. Severity of inflammation caused by genetic variation could independently modify predisposition to ischemic stroke.…”

Section: Discussionmentioning

confidence: 99%

A Meta-Analysis of Candidate Gene Polymorphisms and Ischemic Stroke in 6 Study Populations

Wang¹,

Cheng²,

Brophy³

et al. 2009

Stroke

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patients and 6560 control subjects from 6 case-control association studies conducted in the United States, Europe, and China. Genotyping was performed using the same immobilized probe typing system and meta-analyses were based on summary logistic regressions for each study. The primary analyses were fixed-effects meta-analyses adjusting for age and sex with additive, dominant, and recessive models of inheritance. Results-Although 7 polymorphisms showed a nominal additive association, none remained statistically significant after adjustment for multiple comparisons. In contrast, after stratification for hypertension, 2 lymphotoxin-alpha polymorphisms, which are in strong linkage disequilibrium, were significantly associated among nonhypertensive individuals: LTA 252AϾG (additive model; OR, 1.41 with 95% CI, 1.20 to 1.65; Pϭ0.00002) and LTA 26ThrϾAsn (OR, 1.19 with 95% CI, 1.06 to 1.34; Pϭ0.003). LTA 252AϾG remained significant after adjustment for multiple testing using either the false discovery rate or by permutation testing. The 2 single nucleotide polymorphisms showed no association in hypertensive subjects (eg, LTA 252AϾG, OR, 0.93; 95% CI, 0.84 to 1.03; Pϭ0.17). Conclusions-These

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Section: Discussionmentioning

confidence: 99%

A Meta-Analysis of Candidate Gene Polymorphisms and Ischemic Stroke in 6 Study Populations

Wang¹,

Cheng²,

Brophy³

et al. 2009

Stroke

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“…Other studies support a direct role of the p38 MAPK system in the production of VEGF. Blockade of VEGF by the soluble VEGF receptor 1 (sFlt-1) gene transfer has been shown to attenuate the AngII induced inflammation and remodeling [142].…”

Section: Angii Bronchial Hyperresponsiveness and Airway Remodelingmentioning

confidence: 99%

Local Renin-Angiotensin II Systems, Angiotensin-Converting Enzyme and its Homologue ACE2: Their Potential Role in the Pathogenesis of Chronic Obstructive Pulmonary Diseases, Pulmonary Hypertension and Acute Respiratory Distress Syndrome

Kaparianos¹,

Argyropoulou²

2011

CMC

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Renin-angiotensin II-aldosterone axis has long been known as a regulator of blood pressure and fluid homeostasis. Yet, local renin-angiotensin II systems have been discovered and novel actions of angiotensin II (AngII) have emerged among which its ability to act as a immunomodulator and profibrotic molecule. The enzyme responsible for its synthesis, Angiotensin-converting-enzyme (ACE), is present in high concentrations in lung tissue. In the present paper, we review data from studies of the past decade that implicate AngII and functional polymorphisms of the ACE gene that increase ACE activity with increased susceptibility for asthma and chronic obstructive pulmonary disease (COPD) and for pulmonary hypertension. Moreover, drugs that inhibit the synthesis of AngII (ACE inhibitors) or that antagonize its actions on its receptors (Angiotensin II receptor blockers -ARBs) have been shown to provide beneficial effects. Another recent discovery reviewed is the presence of a homologue of ACE, ACE2, which cleaves a single amino acid from AngII and forms a heptapeptide with vasodilatory actions, Ang 1-7. The balance between ACE and ACE2 is crucial for controlling AngII levels. ACE and ACE2 also appear to modify the severity of Acute Respiratory Distress Syndrome (ARDS), with ACE2 playing a protective role. Finally, mention is made to the recent discovery of ACE2 as a receptor for the SARS Corona Virus.

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“…45,46 The importance of local mediators in inflammation was demonstrated in experimental models, in which VEGF inhibition attenuated Ang II-mediated inflammation and remodeling without influencing Ang-II-induced blood pressure elevation. 46,47 …”

Section: Vascular Permeability and Inflammationmentioning

confidence: 99%

Essential Hypertension

Androulakis

Tousoulis

Papageorgiou

et al. 2009

Cardiology in Review

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Inflammation is a key feature in the initiation, progression, and clinical implications of cardiovascular disorders, including essential hypertension. Increasing evidence shows that activation of renin-angiotensin-aldosterone system and enhanced local production of angiotensin II have been implicated in the pathophysiology of inflammation. Besides being a potent vasoactive peptide, angiotensin II regulates the inflammatory process. Specifically, it increases vascular permeability, participates in the recruitment of inflammatory cells and their adhesion to the activated endothelium, and regulates cell growth and fibrosis. Reactive oxygen species are implicated at every stage in inflammation and activate multiple intracellular signaling molecules and transcription factors associated with inflammatory responses, such as nuclear factor-kappa B and activator protein-1. Other components of the renin-angiotensin-aldosterone system, including aldosterone and/or mineralocorticoid receptor, induce the production of reactive oxygen species and participate in vascular inflammation. Several studies suggest a role of endothelin-1 as an important mediator of chronic inflammation and there is an increasing interest in the relationship between endothelin-1 and reactive oxygen species. These data may have great impact on future therapeutic strategies.

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Is Vascular Endothelial Growth Factor a Missing Link Between Hypertension and Inflammation?

Cited by 14 publications

References 15 publications

A Meta-Analysis of Candidate Gene Polymorphisms and Ischemic Stroke in 6 Study Populations

A Meta-Analysis of Candidate Gene Polymorphisms and Ischemic Stroke in 6 Study Populations

Local Renin-Angiotensin II Systems, Angiotensin-Converting Enzyme and its Homologue ACE2: Their Potential Role in the Pathogenesis of Chronic Obstructive Pulmonary Diseases, Pulmonary Hypertension and Acute Respiratory Distress Syndrome

Essential Hypertension

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