Journal
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
Volume 302, Issue 6, Pages L512-L520Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00289.2011
Keywords
nitric oxide synthases; L-NAME; TRAP
Categories
Funding
- National Institutes of Health [HL-081064, HL-107147, HL-095181, RR026231]
- Ohio Department of Development [BRCP 08-049]
- National Institutes of Health, National Center for Research Resources
- CTSA [1UL1RR024989]
- Cleveland, Ohio
- American Heart Association [0826095H]
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Aytekin M, Aulak KS, Haserodt S, Chakravarti R, Cody J, Minai OA, Dweik RA. Abnormal platelet aggregation in idiopathic pulmonary arterial hypertension: role of nitric oxide. Am J Physiol Lung Cell Mol Physiol 302: L512-L520, 2012. First published January 13, 2012; doi:10.1152/ajplung.00289.2011.-Idiopathic pulmonary arterial hypertension (IPAH) is a rare and progressive disease. Several processes are believed to lead to the fatal progressive pulmonary arterial narrowing seen in IPAH including vasoconstriction, cellular proliferation inflammation, vascular remodeling, abnormalities in the lung matrix, and in situ thrombosis. Nitric oxide (NO) produced by NO synthases (NOS) is a potent vasodilator and plays important roles in many other processes including platelet function. Reduced NO levels in patients with IPAH are known to contribute to the development of pulmonary hypertension and its complications. Platelet defects have been implied in IPAH, but original research supporting this hypothesis has been limited. Normal platelets are known to have NOS activity, but little is known about NOS expression and NO production by platelets in patients with IPAH. Here we characterized the phenotype of the platelets in IPAH and show a defect in their ability to be activated in vitro by thrombin receptor activating protein but not adenosine diphosphate. We also show that endothelial NOS (eNOS) levels in these platelets are reduced and demonstrate that NO is an important regulator of platelet function. Thus reduced levels of eNOS in platelets could impact their ability to regulate their own function appropriately.
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