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10.1161/01.CIR.0000151516.84238.37 http://scihub22266oqcxt.onion/10.1161/01.CIR.0000151516.84238.37 15611366!ä!15611366 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=15611366&cmd=llinks): Failed to open stream: HTTP request failed! 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Aldosteronism and a proinflammatory vascular phenotype: role of Mg2+, Ca2+, and H2O2 in peripheral blood mononuclear cells |pdf=|usr=}}{{15611366}} gab.com Text Aldosteronism and a proinflammatory vascular phenotype: role of Mg2+, Ca2+, and H2O2 in peripheral blood mononuclear cells JO: Circulation http://www.kidney.de/pget.php?&tw=1&pmid=15611366 #FOAvip BACKGROUND: Chronic, inappropriate (relative to dietary Na+) elevations in circulating aldosterone, such as occur in congestive heart failure, are accompanied by a proinflammatory vascular phenotype involving the coronary and systemic vasculature. An immunostimulatory state with activated peripheral blood mononuclear cells (PBMCs) precedes this phenotype and is induced by a fall in cytosolic free [Mg2+]i and subsequent Ca2+ loading of these cells and transduced by oxidative/nitrosative stress. METHODS AND RESULTS: We sought to further validate this hypothesis in rats with aldosterone/1%NaCl treatment (ALDOST) by using several interventions as cotreatment: a Mg2+-supplemented diet; amlodipine, a CCB; and N-acetylcysteine, an antioxidant. Blood samples were obtained at weeks 1 to 4 of ALDOST to monitor [Mg2+]i, [Ca2+]I, and H2O2 production in PBMCs. Coronal ventricular sections were examined for invading inflammatory cells and 3-nitrotyrosine labeling, a marker of oxidative/nitrosative stress. In response to ALDOST and compared with untreated controls, we found an early and persistent reduction in [Mg2+]i with a subsequent rise in [Ca2+]i and H2O2 production, each of which was either attenuated or abrogated by the Mg2+-supplemented diet and by N-acetylcysteine, whereas amlodipine prevented Ca2+ loading and an altered redox state. Cotreatment with these interventions either markedly attenuated or prevented the appearance of the proinflammatory coronary vascular phenotype and the presence of 3-nitrotyrosine in invading inflammatory cells. CONCLUSIONS: We suggest that the immunostimulatory state that appears during aldosteronism and leads to a proinflammatory coronary vascular phenotype is induced by a fall in [Mg2+]i with Ca2+ loading of PBMCs and is transduced by H2O2 production in these cells. Twit Text FOAVip Aldosteronism and a proinflammatory vascular phenotype: role of Mg2+, Ca2+, and H2O2 in peripheral blood mononuclear cells ????Circulation http://www.kidney.de/pget.php?&tw=1&pmid=15611366 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=15611366 #FOAvip English Wikipedia <ref>{{Cite pmid|15611366}}</ref> Aldosteronism and a proinflammatory vascular phenotype: role of Mg2+, Ca2+, and H2O2 in peripheral blood mononuclear cells #MMPMID15611366 Ahokas RA; Sun Y; Bhattacharya SK; Gerling IC; Weber KT Circulation 2005[Jan]; 111 (1): 51-7 PMID15611366show ga BACKGROUND: Chronic, inappropriate (relative to dietary Na+) elevations in circulating aldosterone, such as occur in congestive heart failure, are accompanied by a proinflammatory vascular phenotype involving the coronary and systemic vasculature. An immunostimulatory state with activated peripheral blood mononuclear cells (PBMCs) precedes this phenotype and is induced by a fall in cytosolic free [Mg2+]i and subsequent Ca2+ loading of these cells and transduced by oxidative/nitrosative stress. METHODS AND RESULTS: We sought to further validate this hypothesis in rats with aldosterone/1%NaCl treatment (ALDOST) by using several interventions as cotreatment: a Mg2+-supplemented diet; amlodipine, a CCB; and N-acetylcysteine, an antioxidant. Blood samples were obtained at weeks 1 to 4 of ALDOST to monitor [Mg2+]i, [Ca2+]I, and H2O2 production in PBMCs. Coronal ventricular sections were examined for invading inflammatory cells and 3-nitrotyrosine labeling, a marker of oxidative/nitrosative stress. In response to ALDOST and compared with untreated controls, we found an early and persistent reduction in [Mg2+]i with a subsequent rise in [Ca2+]i and H2O2 production, each of which was either attenuated or abrogated by the Mg2+-supplemented diet and by N-acetylcysteine, whereas amlodipine prevented Ca2+ loading and an altered redox state. Cotreatment with these interventions either markedly attenuated or prevented the appearance of the proinflammatory coronary vascular phenotype and the presence of 3-nitrotyrosine in invading inflammatory cells. CONCLUSIONS: We suggest that the immunostimulatory state that appears during aldosteronism and leads to a proinflammatory coronary vascular phenotype is induced by a fall in [Mg2+]i with Ca2+ loading of PBMCs and is transduced by H2O2 production in these cells. |Acetylcysteine/pharmacology/therapeutic use[MESH] |Amlodipine/pharmacology/therapeutic use[MESH] |Animals[MESH] |Biomarkers[MESH] |Body Weight/drug effects[MESH] |Calcium/blood/*physiology[MESH] |Dietary Supplements[MESH] |Hydrogen Peroxide/*blood[MESH] |Hyperaldosteronism/*complications/immunology/metabolism[MESH] |Leukocytes, Mononuclear/*metabolism[MESH] |Magnesium/administration & dosage/blood/*physiology/therapeutic use[MESH] |Male[MESH] |Oxidation-Reduction[MESH] |Oxidative Stress/drug effects[MESH] |Phenotype[MESH] |Rats[MESH] |Rats, Sprague-Dawley[MESH] |Sodium Chloride, Dietary/toxicity[MESH] |Tyrosine/*analogs & derivatives/analysis[MESH]Aldosteronism and a proinflammatory vascular phenotype: role of Mg2+, (epmc).pdf DeepDyve Pubget Overpricing