Endothelial dysfunction, nitric oxide and platelet activation in hypertensive and diabetic type II patients

Alterations in the synthesis or enhanced inactivation of nitric oxide (NO) and an increase in endothelin-1 production lead to an imbalance that can induce arterial hypertension. Type II diabetes is characterized by impaired endothelium-dependent vasodilation and vascular disease. NO is produced thro...

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Autor principal: Ouvia, S.M
Otros Autores: La Greca, R.D, Zanaro, N.L, Palmer, L., Sassetti, B.
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: 2001
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Acceso en línea:Registro en Scopus
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024 7 |2 scopus  |a 2-s2.0-0035871024 
024 7 |2 cas  |a Nitric Oxide, 10102-43-9; Tumor Necrosis Factor-alpha; von Willebrand Factor 
040 |a Scopus  |b spa  |c AR-BaUEN  |d AR-BaUEN 
030 |a THBRA 
100 1 |a Ouvia, S.M. 
245 1 0 |a Endothelial dysfunction, nitric oxide and platelet activation in hypertensive and diabetic type II patients 
260 |c 2001 
270 1 0 |m Sassetti, B.; Departamento de Quimica Biologica, Fac. de Ciencias Exactas y Naturales, Universidad de Buenos Aires, 4 Piso, 1428 Buenos Aires, Argentina; email: sassetti@qb.fcen.uba.ar 
506 |2 openaire  |e Política editorial 
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504 |a Vallejo, S., Angulo, J., Periro, C., Nevado, J., Sanchez-Ferrer, A., Petidier, R., Sanchez-Ferrer, C.F., Rodriguez-Manas, L., Highly glycated oxyhaemoglobin impairs nitric oxide relaxations in human mesenteric microvessels (2000) Diabetologia, 43, pp. 83-90 
520 3 |a Alterations in the synthesis or enhanced inactivation of nitric oxide (NO) and an increase in endothelin-1 production lead to an imbalance that can induce arterial hypertension. Type II diabetes is characterized by impaired endothelium-dependent vasodilation and vascular disease. NO is produced through L-arginine pathway by three different isoforms of nitric oxide synthase (NOS), an inducible form that can be activated by cytokines such as tumor necrosis factor α (TNFα). We evaluated NO plasmatic levels, endothelial damage markers such as von Willebrand factor (vWF), platelet activation, soluble P-selectin (sP-Sel), TNFα levels, insulinaemia (I), glycosylated haemoglobin (HbA1c), glycaemia and blood pressure in 32 hypertensive diabetic type II patients (Group A), 37 hypertensive patients (Group B) and 35 healthy subjects (Group C) matched in sex, age, body mass index and dietary habits. The level of I was increased in patients compared to the controls and correlated with their NO levels. vWF plasmatic levels were increased in Group A compared to Groups B and C. We also found significant differences in platelet activation among all the groups. In diabetic patients, increased NO levels correlated with TNFα, HbA1c and platelet activation showed greater endothelial damage than in Group B. These parameters described a prothrombotic state associated with an insulin resistance state, an increased vWF release, raised sP-Sel and TNFα levels and, maybe, low NO bioavailability, which could lead to a higher risk of development of thrombotic events in hypertensive diabetic patients (Group A) than in the hypertensive patients in Group B. © 2001 Elsevier Science Ltd.  |l eng 
536 |a Detalles de la financiación: Universidad de Buenos Aires, UBACYT TX22 
536 |a Detalles de la financiación: This work was supported by the Universidad de Buenos Aires, grant UBACYT TX22. 
593 |a Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina 
593 |a Hospital Churruca Visca, Buenos Aires, Argentina 
593 |a Departamento de Qumica, Biolgica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Ciudad Universitaria, Pab. II, Piso, 1428 Buenos Aires, Argentina 
650 1 7 |2 spines  |a DIABETES 
690 1 0 |a ENDOTHELIAL DYSFUNCTION 
690 1 0 |a HYPERTENSION 
690 1 0 |a NITRIC OXIDE 
690 1 0 |a PLATELET ACTIVATION 
690 1 0 |a VON WILLEBRAND FACTOR 
690 1 0 |a ARGININE 
690 1 0 |a ENDOTHELIN 1 
690 1 0 |a GLYCOSYLATED HEMOGLOBIN 
690 1 0 |a NITRIC OXIDE 
690 1 0 |a NITRIC OXIDE SYNTHASE 
690 1 0 |a PADGEM PROTEIN 
690 1 0 |a TUMOR NECROSIS FACTOR ALPHA 
690 1 0 |a VON WILLEBRAND FACTOR 
690 1 0 |a ADULT 
690 1 0 |a AGED 
690 1 0 |a ARTICLE 
690 1 0 |a BIOAVAILABILITY 
690 1 0 |a BLOOD PRESSURE 
690 1 0 |a BODY MASS 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a DIET 
690 1 0 |a DISEASE MARKER 
690 1 0 |a ENDOTHELIUM LESION 
690 1 0 |a ENZYME ACTIVATION 
690 1 0 |a FEMALE 
690 1 0 |a GLUCOSE BLOOD LEVEL 
690 1 0 |a HUMAN 
690 1 0 |a HYPERTENSION 
690 1 0 |a INSULIN BLOOD LEVEL 
690 1 0 |a INSULIN RESISTANCE 
690 1 0 |a INSULINEMIA 
690 1 0 |a MAJOR CLINICAL STUDY 
690 1 0 |a MALE 
690 1 0 |a NON INSULIN DEPENDENT DIABETES MELLITUS 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a PROTEIN BLOOD LEVEL 
690 1 0 |a THROMBOCYTE ACTIVATION 
690 1 0 |a VASODILATATION 
690 1 0 |a AGED 
690 1 0 |a BLOOD PRESSURE 
690 1 0 |a CASE-CONTROL STUDIES 
690 1 0 |a DIABETES MELLITUS, TYPE 2 
690 1 0 |a ENDOTHELIUM, VASCULAR 
690 1 0 |a FEMALE 
690 1 0 |a HUMANS 
690 1 0 |a HYPERTENSION 
690 1 0 |a MALE 
690 1 0 |a MIDDLE AGED 
690 1 0 |a NITRIC OXIDE 
690 1 0 |a PLATELET ACTIVATION 
690 1 0 |a THROMBOPHILIA 
690 1 0 |a TUMOR NECROSIS FACTOR-ALPHA 
690 1 0 |a VON WILLEBRAND FACTOR 
700 1 |a La Greca, R.D. 
700 1 |a Zanaro, N.L. 
700 1 |a Palmer, L. 
700 1 |a Sassetti, B. 
773 0 |d 2001  |g v. 102  |h pp. 107-114  |k n. 2  |p Thromb. Res.  |x 00493848  |t Thrombosis Research 
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