Angiotensin Induces Inflammatory Activation of Human Vascular Smooth Muscle Cells

Kranzhöfer, Roger; Schmidt, Joachim; Pfeiffer, C; Hagl, S.; Libby, Peter; Kübler, W.

doi:10.1161/01.atv.19.7.1623

Cited by 432 publications

(284 citation statements)

References 56 publications

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“…Dechend et al reported that AT 1 -AAs induced signaling in vascular cells including AP-1 and NF-κB activation (10,11). Both of these nuclear factors participate in inflammation (23,24). Wallukat et al found monocytes, which were pivotal to vascular wall inflammatory processes, could be stimulated by AT 1 -AAs to adhere, produce tissue factor, and probably reactive oxygen species (25).…”

Section: Discussionmentioning

confidence: 99%

Agonistic AT1 Receptor Autoantibody Increases in Serum of Patients with Refractory Hypertension and Improves Ca2+ Mobilization in Cultured Rat Vascular Smooth Muscle Cells

et al. 2008

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Agonistic AT 1 receptor autoantibodies (AT 1 -AAs) have been described in the patients with malignant hypertension or preeclampia. Furthermore, AT 1 -AAs were highly associated with refractory hypertension. Function of vascular smooth muscle cells (VSMCs) is important in the regulation of blood pressure. We investigated and compared the ability of angiotensin II (Ang II) and AT 1 -AAs to stimulate the intracellular calcium mobilization and cellular proliferation of rat VSMCs. Twenty-two patients with refractory hypertension, 24 patients with non-refractory hypertension and 37 normotensives were recruited. The serum of each patient was detected for the presence of

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Section: Discussionmentioning

confidence: 99%

Agonistic AT1 Receptor Autoantibody Increases in Serum of Patients with Refractory Hypertension and Improves Ca2+ Mobilization in Cultured Rat Vascular Smooth Muscle Cells

et al. 2008

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“…16 Third, up to 30% of circulating IL-6 is produced by the adipose tissue 17,18 and the relationship between obesity and hypertension is well known. Finally, IL-6 increases collagen synthesis in the vessel wall 19 and reduces its degradation.…”

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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“…74,78 Angiotensin-II is known to increase VCAM-1 expression and the production of inflammatory cytokines that promote atherogenesis 79,80 (Fig. 1).…”

Section: Antihypertensive Medicationsmentioning

confidence: 99%

Current and future concepts in stroke prevention

O’Rourke

Dean

Akhtar

et al. 2004

Canadian Medical Association Journal

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STROKE IS A MAJOR CAUSE OF MORBIDITY and mortality in an aging population. The current understanding of the pathophysiology of atherosclerotic diseases, the most common cause of stroke, and the evidence for existing therapeutic interventions for the prevention of stroke are presented. Specifically, we review the evidence for antiplatelet agents, anticoagulants, antihypertensive medications, lipidlowering agents and carotid endarterectomy for stroke prevention. primary preventive measure, antiplatelet agents do not reduce the risk of ischemic stroke among patients without vascular disease. They are associated with an increased risk of intracranial hemorrhage (odds ratio [OR] 1.35, 95% confidence interval [CI] 0.88-2.10) 23 and major noncerebral hemorrhage (OR 1.73, 95% CI 1.14-2.63 ). 24 The benefits of ASA in the secondary prevention of stroke have been well documented in the period immediately after a stroke 25 (Table 1). Long-term antiplatelet treatment after stroke shows an even more impressive reduction of 25 nonfatal strokes and 36 serious vascular events per 1000 treated over a 29-month follow-up period. 25 There appears to be no difference in efficacy between low (50 mg) and higher doses (up to 1500 mg) of ASA. 29,30 The combination of dipyridamole and ASA has been shown to reduce the relative risk of recurrent stroke compared with ASA alone 26 (Table 1). Dipyridamole inhibits platelet aggregation by increasing levels of cyclic adenosine monophosphate and cyclic guanosine monophosphate. The limiting factor in the use of the ASAdipyridamole combination is the latter's potential effects on coronary perfusion. Dipyridamole can cause coronary vasodilation, which results in increased blood flow to nonstenosed coronary arteries. The result is that myocardial ischemia may be provoked during exercise. As such, the current American College of Cardiology/American Heart Association guidelines recommend that dipyridamole not be used in patients with chronic stable angina. 31 However, this recommendation was based on shortacting dipyridamole, which also reduced myocardial ischemia in a similar number of patients in the study quoted by these guidelines. 32 With the use of sustained-release dipyridamole, no increase in cardiac events was observed in subjects with prior coronary artery disease. 33 Thienopyridines block adenosine-diphosphate-mediated platelet aggregation. Ticlopidine was the first of this class of drug to be studied for stroke prevention. One clinical trial demonstrated that patients treated with ticlopidine had similar rates of stroke as those treated with ASA 28 (Table 1). However, serious granulocytopenia associated with ticlo- Leukocytes localize in the earliest atherosclerotic lesions, binding to vascular cell adhesion molecules (VCAM-1) on the vascular endothelium and migrating into the intima. This initiates and perpetuates a local inflammatory response. Monocytes mature into lipid-scavenging macrophages and subsequently foam cells. T-lymphocytes express inflammatory cytokines, which cont...

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Angiotensin Induces Inflammatory Activation of Human Vascular Smooth Muscle Cells

Cited by 432 publications

References 56 publications

Agonistic AT1 Receptor Autoantibody Increases in Serum of Patients with Refractory Hypertension and Improves Ca2+ Mobilization in Cultured Rat Vascular Smooth Muscle Cells

Agonistic AT1 Receptor Autoantibody Increases in Serum of Patients with Refractory Hypertension and Improves Ca2+ Mobilization in Cultured Rat Vascular Smooth Muscle Cells

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

Current and future concepts in stroke prevention

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