Background: Recent studies have revealed a higher rate of cardiovascular complications in primary aldosteronism (PA) compared to patients with essential hypertension (EH). Asymmetric dimethylarginine (ADMA) is a marker of endothelial dysfunction that could contribute to increased cardiovascular risk in patients with PA.
Objectives: The aim of this study was to compare the levels of ADMA among patients with PA, controls with EH and healthy participants. Methods: Serum ADMA levels were determined, using commercially available competitive enzyme-linked immunosorbent assay.
Methods: Serum ADMA levels were determined, using commercially available competitive enzyme-linked immunosorbent assay.
Results: Patients with PA had significantly higher concentrations of ADMA than healthy controls (0.488 ± 0.085 vs. 0.433 ± 0.053 μmol/L, P = 0.027). No difference was found in ADMA levels between cases with PA and EH (0.488 ± 0.085 vs. 0.476 ± 0.075 μmol/L, р = 0.636). The difference between patients with EH and normotensive controls did not reach statistical significance (P = 0.06).
Conclusions: The lack of difference between ADMA levels in patients with PA and EH suggests that endothelial dysfunction is more likely related to hypertension per se than to the specific etiology of elevated blood pressure.
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http://dx.doi.org/10.5812/ijem.30324 | DOI Listing |
Biomedicines
December 2024
Department of Obstetrics and Gynaecology, Medical University of Graz, Auenbruggerplatz 14, 8036 Graz, Austria.
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Division of Clinical Pharmacology, Department of Pharmacology, Jichi Medical University, Shimotsuke 329-0498, Japan.
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Department of Cardiovascular Surgery, Ageo Central General Hospital, Saitama, Japan.
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December 2024
Department of Radiation Oncology, University of Health Sciences Türkiye, Sisli Hamidiye Etfal Training and Research Hospital, Istanbul, Türkiye.
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View Article and Find Full Text PDFFASEB J
January 2025
Department of Medicine, Rhode Island Hospital and Brown University School of Medicine, Providence, Rhode Island, USA.
Bromodomain-containing protein 4 (BRD4) plays a vital role in fibrosis of various organs. However, the underlying mechanism of BRD4 in renal fibrosis remains unclear. To construct in vitro and in vivo models of renal fibrosis, TCMK-1 cells were subjected to TGF-β1 treatment and mice were subjected to UUO surgery and adenine induction.
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