Impaired fibrinolysis and insulin resistance in patients with hypertension |
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| Institution: | 1. Division of Cardiology, Department of Internal Medicine, and Clinical Research Center, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, Republic of China;2. Division of Endocrinology and Metabolism, Department of Internal Medicine, and Clinical Research Center, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, Republic of China;3. Division of Hematology, Department of Internal Medicine, and Clinical Research Center, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, Republic of China;1. West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, Sichuan 610041, PR China;2. Department of Biomedical Science, Charles E. Schmidt College of Medicine and Brain Institute, Florida Atlantic University, Jupiter, FL 33458, USA;3. Institute for Behavioral Medicine Research, College of Medicine, The Ohio State University, Columbus, OH 43210, USA;4. Division of Biosciences, College of Dentistry, The Ohio State University, Columbus, OH 43210, USA;5. Department of Neuroscience, The Ohio State University, Columbus, OH 43210, USA;6. Department of Animal Science, University of Illinois Urbana-Champaign, Urbana, IL 61801, USA;7. Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Wuhan University, Wuhan, Hubei 430072, PR China;8. Wuhan Hamilton Biotechnology Co., Ltd., Wuhan, Hubei 430075, PR China;9. Department of Neurosurgery, Renmin Hospital, Wuhan University, Wuhan, Hubei 430060, PR China;1. Faculty of Biology, Medicine and Health, University of Manchester, M13 9PT Manchester, UK;2. “Momentum” Laboratory of Neuroimmunology, Institute of Experimental Medicine, Szigony u. 43, 1083 Budapest, Hungary;3. Laboratory of Cerebral Cortex Research, Institute of Experimental Medicine, Szigony u. 43, 1083 Budapest, Hungary;4. Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany;5. Institute of Experimental and Clinical Pharmacology and Toxicology, University of Lübeck, 23538 Lübeck, Germany;6. Department of Infection, Immunity & Cardiovascular Disease, Medical School, University of Sheffield, S10 2RX Sheffield, UK;1. Department of Chemical Biology, Dong-Eui University, Busan 614-714, Republic of Korea;2. Department of Applied Chemistry, Dong-Eui University, Busan 614-714, Republic of Korea;1. Nanophotonics Lab, Department of Physics, Indian Institute of Technology Delhi, Hauz Khas, New Delhi 110016, India;2. Institute for Life Sciences and Department of Chemistry, University of Southampton, Southampton SO17 1BJ, UK |
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| Abstract: | Plasma plasminogen activator inhibitor type 1 (PAI-1) and tissue plasminogen activator (tPA) antigens and activities were measured in 28 patients with hypertension and 12 normal controls. Steady state plasma glucose (SSPG) concentrations were also determined after an infusion of somatostatin, insulin and glucose. Patients with hypertension were further subdivided into two groups: insulin resistance (SSPG > 190 mg/dL, n = 14) and no insulin resistance (SSPG < 190 mg/dL, n = 14). As compared to normal controls, hypertensive patients, either with or without insulin resistance, had significant (P < .005) increases in PAI-1 activity (18.6 ± 1.3 ν 8.1 ± 0.8 IU/mL), PAI-1 antigen (31.1 ± 2.0 ν 12.7 ± 0.9 ng/mL) and tPA antigen (15.5 ± 0.9 ν 8.8 ± 0.9 ng/mL), and significant decrease in tPA activity (0.43 ± 0.05 ν 1.02 ± 0.16 IU/mL) than normotensive controls. Furthermore, hypertensive patients with insulin resistance had significantly higher PAI-1 activity (22.0 ± 2.2 ν 15.3 ± 0.8 IU/mL, P = .006) and tPA antigen (17.4 ± 1.2 ν 13.6 ± 1.3 ng/mL, P = .02) than did hypertensive patients without insulin resistance. However, PAI-1 antigen was insignificantly higher (34.1 ± 2.9 ν 28.1 ± 2.4 ng/mL, P = .06) and tPA activity insignificantly lower (0.42 ± 0.08 ν 0.43 ± 0.08 IU/mL, P = .45) in hypertensive patients with insulin resistance than in those without insulin resistance. In addition, PAI-1 activity and tPA antigen were significantly correlated with blood pressure, SSPG, triglyceride, HDL-cholesterol and integrated glucose response to an oral load of 75 g glucose. Thus, patients with hypertension have impaired fibrinolytic activity due to increased PAI-1 when compared to normotensive controls, and the magnitude of this fibrinolytic defect is greater in hypertensive patients who have insulin resistance. Insulin resistance with associated metabolic abnormalities may be one of the causes for impaired fibrinolysis in hypertension. |
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