Nitric oxide activity in platelets of dengue haemorrhagic fever patients: the apparent paradoxical role of ADMA and l-NMMA

Dengue haemorrhagic fever (DHF) is a prevalent acute disease that occurs in patients infected by an arbovirus in tropical and subtropical regions. We have previously shown increased intraplatelet nitric oxide (NO) production in patients with dengue fever associated with reduced platelet aggregation....

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Bibliographic Details
Published in:Transactions of the Royal Society of Tropical Medicine and Hygiene 2012-03, Vol.106 (3), p.174-179
Main Authors: Matsuura, Cristiane, Moraes, Thalyta L., Barbosa, Julia B., Moss, Monique B., Siqueira, Mariana A.S., Mann, Giovanni E., Neto, Miguel Lemos, Brunini, Tatiana M.C., Mendes-Ribeiro, Antonio Claudio
Format: Article
Language:English
Subjects:
Adult
Arboviral haemorrhagic fevers
Arboviroses
Arginine
Arginine - analogs & derivatives
Arginine - blood
Arginine - pharmacology
Arginine analogues
Biological and medical sciences
Blood platelets
Blood Platelets - drug effects
Brazil
Dengue fevers
Dengue haemorrhagic fever
Enzyme Inhibitors - pharmacology
Female
General aspects
Human viral diseases
Humans
Infectious diseases
Male
Medical sciences
Nitric oxide
Nitric Oxide Synthase
omega-N-Methylarginine - pharmacology
Platelet Aggregation
Severe Dengue - blood
Severe Dengue - complications
Severe Dengue - drug therapy
Thrombocytopenia
Thrombocytopenia - blood
Thrombocytopenia - drug therapy
Thrombocytopenia - etiology
Tropical viral diseases
Viral diseases
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Summary:Dengue haemorrhagic fever (DHF) is a prevalent acute disease that occurs in patients infected by an arbovirus in tropical and subtropical regions. We have previously shown increased intraplatelet nitric oxide (NO) production in patients with dengue fever associated with reduced platelet aggregation. In this study, l-arginine transport as well as expression and activity of nitric oxide synthase (NOS) isoforms in the presence or absence of l-arginine analogues were examined in 23 DHF patients. l-arginine transport and NOS activity in platelets were increased in patients with DHF compared with controls. However, platelet endothelial NOS (eNOS) and inducible (iNOS) protein levels did not differ between healthy controls and DHF patients. Endogenous or exogenous analogues did not inhibit platelet NOS activity from DHF patients. In contrast, endogenous l-arginine analogues [NG-monomethyl-l-arginine (l-NMMA) and asymmetric dimethylarginine (ADMA)] inhibited NOS activity in platelets from healthy subjects. These results show the first evidence that the intraplatelet l-arginine–NO pathway is activated in DHF patients. The lack of inhibition of NO formation in vitro by all l-arginine analogues tested in DHF platelets may suggest another mechanism by which NOS activity can be regulated.
ISSN:0035-9203
1878-3503
DOI:10.1016/j.trstmh.2011.10.009