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Cardiovascular Research 2003 57(1):109-118; doi:10.1016/S0008-6363(02)00657-0
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Endothelin-1 induced proinflammatory markers in the myocardium and leukocytes of guinea-pigs

Role of glycoprotein IIB/IIIA receptors

Laura Molero, Jeronimo Farré, Antonio García-Mendez, Petra Jiménez Mateos-Caceres, Carolina Carrasco Martín, Inmaculada Millás, Felipe Navarro, Manuel Córdoba, Santos Casado and Antonio López-Farré*

Cardiovascular Research Laboratory, Fundación Jiménez Díaz, Av. Reyes Católicos, 2, Madrid, 28040 Spain

* Corresponding author. Tel.: +34-91-550-4821 alopeza{at}fjd.es

Aim:To assess whether endothelin-1 (ET-1) induces the in vivo expression of inflammatory-related proteins, namely cyclooxygenase-2 (COX-2) and tissue factor, in the myocardium and circulating leukocytes of guinea-pigs. The involvement of platelets was also analyzed. Methods: ET-1 (0.013 µg/min) was infused to male guinea-pigs for 45 min in the presence and absence of tirofiban, a nonpeptidic blocker of the glycoprotein IIb/IIIa receptor (GPIIb/IIIa). Tissue factor and COX-2 expression were determined by Western blot. Results: No changes in mean arterial pressure and heart rate were detected. ET-1-infused guinea-pigs showed a marked increase in the number of platelets expressing activated GPIIb/IIIa receptors (0.8±0.03% vs. 6.5±0.2%; P<0.05). Tirofiban (10 µg/Kg bw/min) blunted ex vivo platelet aggregation in response to ADP, although only partially reduced COX-2 and tissue factor expression in both the myocardium and leukocytes of ET-1-infused guinea-pigs. The myocardium of platelet-depleted guinea-pigs also showed a reduced COX-2 expression after ET-1 infusion (57±3% reduction; P<0.05). In vitro studies demonstrated that platelets (107 and 109 platelets/well) enhanced ET-1 (10–7 mol/l)-induced COX-2 expression in heart slices. Conclusion: ET-1 stimulated in vivo the expression of the pro-inflammatory proteins COX-2 and tissue factor in the myocardium and in leukocytes by a mechanism GPIIb/IIIa platelet receptors.

KEYWORDS Endothelial factors; Endothelins; Infection/inflammation; Leukocytes; Myocytes; Platelets


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