ArticleHypertension (Dallas, Tex. : 1979)2015
Low-Dose Mineralocorticoid Receptor Blockade Prevents Western Diet-Induced Arterial Stiffening in Female Mice.
Registry-linked trialOpen access · bronzeAbstract read
In one paragraph
Article in Hypertension (Dallas, Tex. : 1979), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05593055 (Mineralocorticoid Receptor, Coronary Microvascular Function, and Cardiac Efficiency in Hypertension), which is not on this map. Cited by 97 papers.
0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
13.2field-weighted citation impact, top 1% of its field
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Mineralocorticoid Receptor, Coronary Microvascular Function, and Cardiac Efficiency in Hypertension
Who cites it
97 citing papers in PubMed, 149 citations in OpenAlex.
- Circuit training on oxidative stress and arterial health: a health promotion perspective for obese adult men.Frontiers in public health · 2025Trial
- Targeting the aldosterone-mineralocorticoid receptor pathway in cardiovascular-kidney-metabolic syndrome.Nature reviews. Nephrology · 2026Review
- Guidelines for evaluating endothelial function in vascular tissue.American journal of physiology. Heart and circulatory physiology · 2026Review
- Mineralocorticoid and estrogen receptors as sex-dependent modulators of vascular health in aging and obesity.The Journal of pharmacology and experimental therapeutics · 2025Review
- Metabolic and vascular insulin resistance: partners in the pathogenesis of cardiovascular disease in diabetes.American journal of physiology. Heart and circulatory physiology · 2025Review
- Review
- Vasomotor responses are similar between outbred UM-HET3 and inbred C57BL/6J male and female mouse mesenteric resistance arteries.Frontiers in physiology · 2025Article
- Long-Term Time in Target Range for Systolic Blood Pressure Since Childhood and Midlife Arterial Stiffness.JACC. Asia · 2025Article
- PAI-1 Regulates the Cytoskeleton and Intrinsic Stiffness of Vascular Smooth Muscle Cells.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Role of L-type CaPhysiological reports · 2024Article
- The mineralocorticoid receptor in diabetic kidney disease.American journal of physiology. Renal physiology · 2024Review
- Diabetic Vasculopathy: Molecular Mechanisms and Clinical Insights.International journal of molecular sciences · 2024Review
- Vascular endothelial mineralocorticoid receptors and epithelial sodium channels in metabolic syndrome and related cardiovascular disease.Journal of molecular endocrinology · 2023Review
- Sex differences in weight gain, blood pressure control, and responses to melanocortin-4 receptor antagonism in offspring from lean and obese parents.American journal of physiology. Regulatory, integrative and comparative physiology · 2023Article
- Vascular function in hypertension: does gender dimension matter?Journal of human hypertension · 2023Review
- Endothelial MRs Mediate Western Diet-Induced Lipid Disorders and Skeletal Muscle Insulin Resistance in Females.Endocrinology · 2023Article
- Multi-omic analysis of the cardiac cellulome defines a vascular contribution to cardiac diastolic dysfunction in obese female mice.Basic research in cardiology · 2023Article
- Cardiovascular Disease in Obstructive Sleep Apnea: Putative Contributions of Mineralocorticoid Receptors.International journal of molecular sciences · 2023Review
- Dissociation of pulse wave velocity and aortic wall stiffness in diabetic db/db mice: The influence of blood pressure.Frontiers in physiology · 2023Article
- Endothelial cell-specific mineralocorticoid receptor activation promotes diastolic dysfunction in diet-induced obese male mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2023Article
37 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 1 institution in 1 country.
Vincent G DeMarcoFrom the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine (V.G.D., J.H., G.J., A.R.A., M.G., M.R.H., C.M., J.R.S.), Division of Nephrology, Department of Medicine (A.W.-C.), Department of Medical Pharmacology and Physiology (V.G.D., F.I.R.-P., L.A.M.-L., Z.S., G.A.M., J.R.S.), and Department of Biomedical Sciences (S.B.B.), University of Missouri Columbia School of Medicine; Research Service, Harry S. Truman Memorial Veterans Hospital, Columbia, MO (V.G.D., J.H., G.J., A.R.A., S.B.B., M.G., M.R.H., C.M., A.W.-C., J.R.S.); and Dalton Cardiovascular Research Center, Columbia, MO (F.I.R.-P., L.A.M.-L., S.B.B., Z.S., G.A.M.). demarcov@missouri.edu sowersj@missouri.edu.
Javad HabibiFrom the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine (V.G.D., J.H., G.J., A.R.A., M.G., M.R.H., C.M., J.R.S.), Division of Nephrology, Department of Medicine (A.W.-C.), Department of Medical Pharmacology and Physiology (V.G.D., F.I.R.-P., L.A.M.-L., Z.S., G.A.M., J.R.S.), and Department of Biomedical Sciences (S.B.B.), University of Missouri Columbia School of Medicine; Research Service, Harry S. Truman Memorial Veterans Hospital, Columbia, MO (V.G.D., J.H., G.J., A.R.A., S.B.B., M.G., M.R.H., C.M., A.W.-C., J.R.S.); and Dalton Cardiovascular Research Center, Columbia, MO (F.I.R.-P., L.A.M.-L., S.B.B., Z.S., G.A.M.).
Guanghong JiaFrom the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine (V.G.D., J.H., G.J., A.R.A., M.G., M.R.H., C.M., J.R.S.), Division of Nephrology, Department of Medicine (A.W.-C.), Department of Medical Pharmacology and Physiology (V.G.D., F.I.R.-P., L.A.M.-L., Z.S., G.A.M., J.R.S.), and Department of Biomedical Sciences (S.B.B.), University of Missouri Columbia School of Medicine; Research Service, Harry S. Truman Memorial Veterans Hospital, Columbia, MO (V.G.D., J.H., G.J., A.R.A., S.B.B., M.G., M.R.H., C.M., A.W.-C., J.R.S.); and Dalton Cardiovascular Research Center, Columbia, MO (F.I.R.-P., L.A.M.-L., S.B.B., Z.S., G.A.M.).
Annayya R AroorFrom the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine (V.G.D., J.H., G.J., A.R.A., M.G., M.R.H., C.M., J.R.S.), Division of Nephrology, Department of Medicine (A.W.-C.), Department of Medical Pharmacology and Physiology (V.G.D., F.I.R.-P., L.A.M.-L., Z.S., G.A.M., J.R.S.), and Department of Biomedical Sciences (S.B.B.), University of Missouri Columbia School of Medicine; Research Service, Harry S. Truman Memorial Veterans Hospital, Columbia, MO (V.G.D., J.H., G.J., A.R.A., S.B.B., M.G., M.R.H., C.M., A.W.-C., J.R.S.); and Dalton Cardiovascular Research Center, Columbia, MO (F.I.R.-P., L.A.M.-L., S.B.B., Z.S., G.A.M.).
Francisco I Ramirez-PerezFrom the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine (V.G.D., J.H., G.J., A.R.A., M.G., M.R.H., C.M., J.R.S.), Division of Nephrology, Department of Medicine (A.W.-C.), Department of Medical Pharmacology and Physiology (V.G.D., F.I.R.-P., L.A.M.-L., Z.S., G.A.M., J.R.S.), and Department of Biomedical Sciences (S.B.B.), University of Missouri Columbia School of Medicine; Research Service, Harry S. Truman Memorial Veterans Hospital, Columbia, MO (V.G.D., J.H., G.J., A.R.A., S.B.B., M.G., M.R.H., C.M., A.W.-C., J.R.S.); and Dalton Cardiovascular Research Center, Columbia, MO (F.I.R.-P., L.A.M.-L., S.B.B., Z.S., G.A.M.).
Luis A Martinez-LemusFrom the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine (V.G.D., J.H., G.J., A.R.A., M.G., M.R.H., C.M., J.R.S.), Division of Nephrology, Department of Medicine (A.W.-C.), Department of Medical Pharmacology and Physiology (V.G.D., F.I.R.-P., L.A.M.-L., Z.S., G.A.M., J.R.S.), and Department of Biomedical Sciences (S.B.B.), University of Missouri Columbia School of Medicine; Research Service, Harry S. Truman Memorial Veterans Hospital, Columbia, MO (V.G.D., J.H., G.J., A.R.A., S.B.B., M.G., M.R.H., C.M., A.W.-C., J.R.S.); and Dalton Cardiovascular Research Center, Columbia, MO (F.I.R.-P., L.A.M.-L., S.B.B., Z.S., G.A.M.).
Shawn B BenderFrom the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine (V.G.D., J.H., G.J., A.R.A., M.G., M.R.H., C.M., J.R.S.), Division of Nephrology, Department of Medicine (A.W.-C.), Department of Medical Pharmacology and Physiology (V.G.D., F.I.R.-P., L.A.M.-L., Z.S., G.A.M., J.R.S.), and Department of Biomedical Sciences (S.B.B.), University of Missouri Columbia School of Medicine; Research Service, Harry S. Truman Memorial Veterans Hospital, Columbia, MO (V.G.D., J.H., G.J., A.R.A., S.B.B., M.G., M.R.H., C.M., A.W.-C., J.R.S.); and Dalton Cardiovascular Research Center, Columbia, MO (F.I.R.-P., L.A.M.-L., S.B.B., Z.S., G.A.M.).
Mona GarroFrom the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine (V.G.D., J.H., G.J., A.R.A., M.G., M.R.H., C.M., J.R.S.), Division of Nephrology, Department of Medicine (A.W.-C.), Department of Medical Pharmacology and Physiology (V.G.D., F.I.R.-P., L.A.M.-L., Z.S., G.A.M., J.R.S.), and Department of Biomedical Sciences (S.B.B.), University of Missouri Columbia School of Medicine; Research Service, Harry S. Truman Memorial Veterans Hospital, Columbia, MO (V.G.D., J.H., G.J., A.R.A., S.B.B., M.G., M.R.H., C.M., A.W.-C., J.R.S.); and Dalton Cardiovascular Research Center, Columbia, MO (F.I.R.-P., L.A.M.-L., S.B.B., Z.S., G.A.M.).
Melvin R HaydenFrom the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine (V.G.D., J.H., G.J., A.R.A., M.G., M.R.H., C.M., J.R.S.), Division of Nephrology, Department of Medicine (A.W.-C.), Department of Medical Pharmacology and Physiology (V.G.D., F.I.R.-P., L.A.M.-L., Z.S., G.A.M., J.R.S.), and Department of Biomedical Sciences (S.B.B.), University of Missouri Columbia School of Medicine; Research Service, Harry S. Truman Memorial Veterans Hospital, Columbia, MO (V.G.D., J.H., G.J., A.R.A., S.B.B., M.G., M.R.H., C.M., A.W.-C., J.R.S.); and Dalton Cardiovascular Research Center, Columbia, MO (F.I.R.-P., L.A.M.-L., S.B.B., Z.S., G.A.M.).
Zhe SunFrom the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine (V.G.D., J.H., G.J., A.R.A., M.G., M.R.H., C.M., J.R.S.), Division of Nephrology, Department of Medicine (A.W.-C.), Department of Medical Pharmacology and Physiology (V.G.D., F.I.R.-P., L.A.M.-L., Z.S., G.A.M., J.R.S.), and Department of Biomedical Sciences (S.B.B.), University of Missouri Columbia School of Medicine; Research Service, Harry S. Truman Memorial Veterans Hospital, Columbia, MO (V.G.D., J.H., G.J., A.R.A., S.B.B., M.G., M.R.H., C.M., A.W.-C., J.R.S.); and Dalton Cardiovascular Research Center, Columbia, MO (F.I.R.-P., L.A.M.-L., S.B.B., Z.S., G.A.M.).
Gerald A MeiningerFrom the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine (V.G.D., J.H., G.J., A.R.A., M.G., M.R.H., C.M., J.R.S.), Division of Nephrology, Department of Medicine (A.W.-C.), Department of Medical Pharmacology and Physiology (V.G.D., F.I.R.-P., L.A.M.-L., Z.S., G.A.M., J.R.S.), and Department of Biomedical Sciences (S.B.B.), University of Missouri Columbia School of Medicine; Research Service, Harry S. Truman Memorial Veterans Hospital, Columbia, MO (V.G.D., J.H., G.J., A.R.A., S.B.B., M.G., M.R.H., C.M., A.W.-C., J.R.S.); and Dalton Cardiovascular Research Center, Columbia, MO (F.I.R.-P., L.A.M.-L., S.B.B., Z.S., G.A.M.).
Camila ManriqueFrom the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine (V.G.D., J.H., G.J., A.R.A., M.G., M.R.H., C.M., J.R.S.), Division of Nephrology, Department of Medicine (A.W.-C.), Department of Medical Pharmacology and Physiology (V.G.D., F.I.R.-P., L.A.M.-L., Z.S., G.A.M., J.R.S.), and Department of Biomedical Sciences (S.B.B.), University of Missouri Columbia School of Medicine; Research Service, Harry S. Truman Memorial Veterans Hospital, Columbia, MO (V.G.D., J.H., G.J., A.R.A., S.B.B., M.G., M.R.H., C.M., A.W.-C., J.R.S.); and Dalton Cardiovascular Research Center, Columbia, MO (F.I.R.-P., L.A.M.-L., S.B.B., Z.S., G.A.M.).
Adam Whaley-ConnellFrom the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine (V.G.D., J.H., G.J., A.R.A., M.G., M.R.H., C.M., J.R.S.), Division of Nephrology, Department of Medicine (A.W.-C.), Department of Medical Pharmacology and Physiology (V.G.D., F.I.R.-P., L.A.M.-L., Z.S., G.A.M., J.R.S.), and Department of Biomedical Sciences (S.B.B.), University of Missouri Columbia School of Medicine; Research Service, Harry S. Truman Memorial Veterans Hospital, Columbia, MO (V.G.D., J.H., G.J., A.R.A., S.B.B., M.G., M.R.H., C.M., A.W.-C., J.R.S.); and Dalton Cardiovascular Research Center, Columbia, MO (F.I.R.-P., L.A.M.-L., S.B.B., Z.S., G.A.M.).
James R SowersFrom the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine (V.G.D., J.H., G.J., A.R.A., M.G., M.R.H., C.M., J.R.S.), Division of Nephrology, Department of Medicine (A.W.-C.), Department of Medical Pharmacology and Physiology (V.G.D., F.I.R.-P., L.A.M.-L., Z.S., G.A.M., J.R.S.), and Department of Biomedical Sciences (S.B.B.), University of Missouri Columbia School of Medicine; Research Service, Harry S. Truman Memorial Veterans Hospital, Columbia, MO (V.G.D., J.H., G.J., A.R.A., S.B.B., M.G., M.R.H., C.M., A.W.-C., J.R.S.); and Dalton Cardiovascular Research Center, Columbia, MO (F.I.R.-P., L.A.M.-L., S.B.B., Z.S., G.A.M.). demarcov@missouri.edu sowersj@missouri.edu.
Harry S. Truman Memorial Veterans' Hospital · US
Funding
Regulation Microvascular: Smooth Muscle Contraction ECM-Integrin-CytoskeletalP01HL095486 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI DAVIS, GEORGE E · 2010 to 2014
$8.4MMechanisms of Microvascular Remodeling ProgressionR01HL088105 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI MARTINEZ-LEMUS, LUIS A · 2009 to 2019
$3.3MANG II OPPOSES INS MEDIATED VASORELAXATION &GLU UTILZAR01HL073101 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI SOWERS, JAMES RUSSELL · 2004 to 2013
$2.7MAng II and Overnutrition and Insulin resistance in Cardiovascular TissueR01HL107910 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI SOWERS, JAMES RUSSELL · 2011 to 2015
$1.8MInteractions of the RAAS and a Western Diet on Insulin Metabolic ActionsI01BX001981 · VA · HARRY S. TRUMAN MEMORIAL VA HOSPITAL · PI LASTRA, GUIDO · 2013 to 2022
–Mineralocorticoid Receptor-Mediated Vascular Insulin ResistanceIK2BX002030 · VA · HARRY S. TRUMAN MEMORIAL VA HOSPITAL · PI BENDER, SHAWN BRADY · 2013 to 2017
–BLRD VA I01 BX001981BLRD VA IK2 BX002030NHLBI NIH HHS P01 HL095486NHLBI NIH HHS R01 HL073101NHLBI NIH HHS R01-HL073101NHLBI NIH HHS R01 HL088105NHLBI NIH HHS R01 HL107910NHLBI NIH HHS R01-HL107910
Abstract
Women are especially predisposed to development of arterial stiffening secondary to obesity because of consumption of excessive calories. Enhanced activation of vascular mineralocorticoid receptors impairs insulin signaling, induces oxidative stress, inflammation, and maladaptive immune responses. We tested whether a subpressor dose of mineralocorticoid receptor antagonist, spironolactone (1 mg/kg per day) prevents aortic and femoral artery stiffening in female C57BL/6J mice fed a high-fat/high-sugar western diet (WD) for 4 months (ie, from 4-20 weeks of age). Aortic and femoral artery stiffness were assessed using ultrasound, pressurized vessel preparations, and atomic force microscopy. WD induced weight gain and insulin resistance compared with control diet-fed mice and these abnormalities were unaffected by spironolactone. Blood pressures and heart rates were normal and unaffected by diet or spironolactone. Spironolactone prevented WD-induced stiffening of aorta and femoral artery, as well as endothelial and vascular smooth muscle cells, within aortic explants. Spironolactone prevented WD-induced impaired aortic protein kinase B/endothelial nitric oxide synthase signaling, as well as impaired endothelium-dependent and endothelium-independent vasodilation. Spironolactone ameliorated WD-induced aortic medial thickening and fibrosis and the associated activation of the progrowth extracellular receptor kinase 1/2 pathway. Finally, preservation of normal arterial stiffness with spironolactone in WD-fed mice was associated with attenuated systemic and vascular inflammation and an anti-inflammatory shift in vascular immune cell marker genes. Low-dose spironolactone may represent a novel prevention strategy to attenuate vascular inflammation, oxidative stress, and growth pathway signaling and remodeling to prevent development of arterial stiffening secondary to consumption of a WD.
Indexed as
AnimalsAortaArteriosclerosisDiet, WesternDose-Response Relationship, DrugEndothelial CellsFemaleFemoral ArteryInflammationMiceMice, Inbred C57BLMineralocorticoid Receptor AntagonistsMyocytes, Smooth MuscleNitric Oxide Synthase Type IIIObesityOxidative StressMineralocorticoid Receptor AntagonistsNitric Oxide Synthase Type IIINos3 protein, mouseReceptors, MineralocorticoidSpironolactonealdosteroneobesityspironolactonevascular stiffness
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Registered trials
NCT05593055ClinicalTrials.gov
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.