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The Effect of Tekturna on Endothelial Function and Endothelial Progenitor Cells in Patients With Early Atherosclerosis

2014-08-27 03:15:56 | BioPortfolio

Summary

We will study the hypothesis that long-term Tekturna treatment will improve endothelial function and the production and function of endothelial progenitor cells (EPCs) in patients with early atherosclerosis. Specifically, long-term Tekturna treatment will increase the Reactive Hyperemia Peripheral Arterial Tonometry indexes and increase the numbers and the function of circulating endothelial progenitor cells, compared to placebo, in association with a reduction in inflammation and oxidative stress.

Study Design

Allocation: Randomized, Control: Placebo Control, Endpoint Classification: Efficacy Study, Intervention Model: Parallel Assignment, Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor), Primary Purpose: Treatment

Conditions

Endothelial Dysfunction

Intervention

Tekturna (Aliskiren), placebo

Location

Mayo Clinic in Rochester
Rochester
Minnesota
United States
55905

Status

Not yet recruiting

Source

Mayo Clinic

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:15:56-0400

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Vitamin D Deficiency in Patients With Hypertension

This study will evaluate the effects of Vitamin D replacement and the effects of an approved medication for hypertension, aliskiren (Tekturna), in patients with high blood pressure who hav...

Trial to Evaluate the Effect of Tektura (Aliskiren), Angiotensin Inhibitors, Diuretics, and Calcium Channel Blockers on Coronary Flow Reserve in Patients With Type II Diabetes and Hypertension

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To assess the efficacy of oral aliskiren (Tekturna) as a therapy for diabetic macular edema

Hemodynamic Effects of Aliskiren Compared to Captopril on the Kidney in Healthy Volunteers on a Low- and High- Sodium Diet

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PubMed Articles [5424 Associated PubMed Articles listed on BioPortfolio]

Direct renin inhibition is not enough to prevent reactive oxygen species generation and vascular dysfunction in renovascular hypertension.

Renin-angiotensin system activation promotes oxidative stress and endothelial dysfunction. However, no previous study has examined the effects of the renin inhibitior aliskiren, either alone or combin...

Interaction of IL-6 and TNF-α contributes to endothelial dysfunction in type 2 diabetic mouse hearts.

Inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), are individually considered as important contributors to endothelial dysfunction in obesity and type 2 diabe...

Diabetic dyslipidaemia is associated with alterations in eNOS, caveolin-1 and endothelial dysfunction in streptozotocin treated rats.

Diabetes is a complex progressive disease characterised by chronic hyperglycaemia and dyslipidaemia associated with endothelial dysfunction. Oxidised LDL (Ox-LDL) is elevated in diabetes and may contr...

Microvascular endothelial dysfunction is associated with albuminuria: the Maastricht Study.

Albuminuria is thought to be a biomarker of microvascular and macrovascular endothelial dysfunction. However, direct evidence for an association of microvascular endothelial dysfunction with albuminur...

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Aliskiren might be beneficial for heart failure. However, the results of various studies are controversial. We conducted a systematic review and meta-analysis to explore the efficacy of aliskiren sup...

Medical and Biotech [MESH] Definitions

A 200-230-kDa tyrosine kinase receptor for vascular endothelial growth factors found primarily in endothelial and hematopoietic cells and their precursors. VEGFR-2 is important for vascular and hematopoietic development, and mediates almost all endothelial cell responses to VEGF.

A vascular endothelial growth factor that specifically binds to VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-2 and VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-3. In addition to being an angiogenic factor it can act on LYMPHATIC VESSELS to stimulate LYMPHANGIOGENESIS. It is similar in structure to VASCULAR ENDOTHELIAL GROWTH FACTOR D in that they both contain N- and C-terminal extensions that were not found in other VEGF family members.

A vascular endothelial growth factor that specifically binds to VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-2 and VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-3. In addition to being an angiogenic factor it can act on LYMPHATIC VESSELS to stimulate LYMPHANGIOGENESIS. It is similar in structure to VASCULAR ENDOTHELIAL GROWTH FACTOR C in that they both contain N- and C-terminal extensions that were not found in other VEGF family members.

A vascular endothelial cell growth factor receptor whose expression is restricted primarily to adult lymphatic endothelium. VEGFR-3 preferentially binds the vascular endothelial growth factor C and vascular endothelial growth factor D and may be involved in the control of lymphangiogenesis.

Misunderstanding among individuals, frequently research subjects, of scientific methods such as randomization and placebo controls.

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