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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Detalles Bibliográficos
Autor principal: Sassetti, Beatriz
Publicado: 2001
Materias:
Diabetes
Endothelial dysfunction
Hypertension
Nitric oxide
Platelet activation
von Willebrand factor
arginine
endothelin 1
glycosylated hemoglobin
nitric oxide
nitric oxide synthase
PADGEM protein
tumor necrosis factor alpha
adult
aged
article
bioavailability
blood pressure
body mass
controlled study
diet
disease marker
endothelium lesion
enzyme activation
female
glucose blood level
human
hypertension
insulin blood level
insulin resistance
insulinemia
major clinical study
male
non insulin dependent diabetes mellitus
priority journal
protein blood level
thrombocyte activation
vasodilatation
Aged
Blood Pressure
Case-Control Studies
Diabetes Mellitus, Type 2
Endothelium, Vascular
Female
Humans
Male
Middle Aged
Nitric Oxide
Platelet Activation
Thrombophilia
Tumor Necrosis Factor-alpha
von Willebrand Factor
Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00493848_v102_n2_p107_Ouvia
http://hdl.handle.net/20.500.12110/paper_00493848_v102_n2_p107_Ouvia
Aporte de:
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires
Descripción
Sumario: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.

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