Platelet hyperaggregability in obesity: is there a role for nitric oxide impairment and oxidative stress?

Summary Epidemiological evidence has shown that platelet activation markers are consistently elevated in obesity, contributing to its prothrombotic state. In order to improve the understanding of the regulation of platelet function in obesity, the aim of this study was to investigate the l‐arginine‐...

Full description

Saved in:
Bibliographic Details
Published in:Clinical and experimental pharmacology & physiology 2016-08, Vol.43 (8), p.738-744
Main Authors: Leite, Natália Rodrigues Pereira, Siqueira de Medeiros, Mariana, Mury, Wanda Vianna, Matsuura, Cristiane, Perszel, Monique Bandeira Moss, Noronha Filho, Gerson, Brunini, Tatiana MC, Mendes-Ribeiro, Antônio Claúdio
Format: Article
Language:English
Subjects:
Adult
Arginine - blood
Blood Platelets - metabolism
cardiovascular disease
Cross-Sectional Studies
Cyclic GMP - blood
Female
Humans
Male
Middle Aged
nitric oxide
Nitric Oxide - metabolism
Nitric Oxide Synthase - blood
obesity
Obesity - blood
Obesity - diagnosis
oxidative stress
Oxidative Stress - physiology
Platelet Aggregation - physiology
platelets
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Summary Epidemiological evidence has shown that platelet activation markers are consistently elevated in obesity, contributing to its prothrombotic state. In order to improve the understanding of the regulation of platelet function in obesity, the aim of this study was to investigate the l‐arginine‐nitric oxide (NO) pathway in obese adults without other cardiovascular risk factor. Seventeen obese (body mass index [BMI] 35.9±1.0 kg/m2) and eighteen age‐matched normal weight subjects (BMI 22.0±0.6 kg/m2) were included in this study. l‐arginine influx was measured with incubation of l‐[3H]‐arginine. NO synthase (NOS) and arginase activities were determined by the citrulline assay and the conversion of l‐[14C]‐arginine to [14C]‐urea, respectively. Cyclic guanosine monophosphate (cGMP) content was evaluated by enzyme‐linked immunosorbent assay. In addition, the study analyzed: platelet aggregation; intraplatelet antioxidant enzymes, via superoxide dismutase (SOD) and catalase activities; and systemic levels of l‐arginine, fibrinogen, and C‐reactive protein (CRP). Obese patients presented a significant decrease of platelet l‐arginine influx, NOS activity, and cGMP levels, along with platelet hyperaggregability. On the presence of NO donor, platelet aggregation was similar between the groups. The fibrinogen and CRP systemic levels were significantly higher and SOD activity was reduced in obesity. No significant differences were observed in plasma levels of l‐arginine and intraplatelet arginase and catalase activities between groups. The diminished NO bioavailability associated with inflammatory status and impaired enzymatic antioxidant defence may contribute to future cardiovascular complications in obesity.
ISSN:0305-1870
1440-1681
DOI:10.1111/1440-1681.12589