Abstract
We evaluated the effect of alacepril, CV-11974, and spironolactone on the production of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha) in cultured human peripheral blood mononuclear cells stimulated with angiotensin (Ang) II. Alacepril, CV-11974, and spironolactone significantly reduced the enhanced production of MCP-1 and TNF-alpha induced by exogenous Ang II. Specifically, 10 muM of spironolactone significantly reduced cytokine production, compared to the same dose of alacepril or CV-11974. These findings indicate that spironolactone may contribute to ameliorate the prognosis of patients with cardiovascular diseases by reducing Ang II-induced inflammation, although further exploration including determining the mechanisms would be required.
MeSH terms
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Adult
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Angiotensin II / antagonists & inhibitors*
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Angiotensin II / pharmacology
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Angiotensin II Type 1 Receptor Blockers / pharmacology
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Angiotensin-Converting Enzyme Inhibitors / pharmacology
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Anti-Inflammatory Agents / pharmacology*
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Benzimidazoles / pharmacology
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Biphenyl Compounds
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Captopril / analogs & derivatives
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Captopril / pharmacology
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Cells, Cultured
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Chemokine CCL2 / metabolism
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Dose-Response Relationship, Drug
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Female
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Humans
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Leukocytes, Mononuclear / drug effects*
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Leukocytes, Mononuclear / metabolism
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Male
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Mineralocorticoid Receptor Antagonists / pharmacology*
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Spironolactone / pharmacology*
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Tetrazoles / pharmacology
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Tumor Necrosis Factor-alpha / metabolism
Substances
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Angiotensin II Type 1 Receptor Blockers
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Angiotensin-Converting Enzyme Inhibitors
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Anti-Inflammatory Agents
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Benzimidazoles
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Biphenyl Compounds
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CCL2 protein, human
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Chemokine CCL2
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Mineralocorticoid Receptor Antagonists
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Tetrazoles
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Tumor Necrosis Factor-alpha
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Angiotensin II
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Spironolactone
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Captopril
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candesartan
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alacepril