Parecoxib increases blood pressure through inhibition of cyclooxygenase-2 messenger RNA in an experimental model

Autores: Vértiz Hernández Ángel Antonio, Martínez Morales Flavio, Valle Aguilera Roberto, López Sánchez Pedro, Villalobos Molina Rafael, Pérez Urizar José Trinidad

Resumen

Background: Cyclooxygenase-2 selective inhibitors have been developed to alleviate pain and inflammation; however, the use of a selective cyclooxygenase-2 inhibitor is associated with mild edema, hypertension, and cardiovascular risk. Aim: To evaluate, in an experimental model in normotensive rats, the effect of treatment with parecoxib in comparison with diclofenac and aspirin and L-NAME, a non-selective nitric oxide synthetase, on mean arterial blood pressure, and cyclooxygenase-1 and -2 messenger RNA and protein expression in aortic tissue. Methods: Rats were treated for seven days with parecoxib (10 mg/kg/day), diclofenac (3.2 mg/kg/day), aspirin (10 mg/kg/day), or L-NAME (10 mg/kg/day). Mean arterial blood pressure was evaluated in rat tail; cyclooxygenase-1 and -2 were evaluated by reverse transcription-polymerase chain reaction and Western blot analysis in aortic tissue. Results: Parecoxib and L-NAME, but not aspirin and diclofenac, increased mean arterial blood pressure by about 50% (p < 0.05) without changes in cardiac frequency. Messenger RNA cyclooxygenase-1 expression in aortic tissue was not modified with any drug (p < 0.05). L-NAME and parecoxib treatment decreased messenger RNA cyclooxygenase-2 and cyclooxygenase-2 (p < 0.05). While cyclooxygenase-1 protein decreased with the three drugs tested but not with L-NAME (p < 0.05), the cyclooxygenase-2 protein decreased only with aspirin and parecoxib (p < 0.05). Conclusion: Parecoxib increases the blood pressure of normotensive rats by the suppression of COX-2 gene expression, which apparently induced cardiovascular control.

Palabras clave: Parecoxib hypertension cyclooxygenase-2 prostaglandin I2 thromboxane A2 mRNA inhibition.

2016-04-18   |   198 visitas   |   Evalua este artículo 0 valoraciones

Vol. 67 Núm.4. Julio-Agosto 2015 Pags. 250-257 Rev Invest Clin 2015; 67(4 ENGLISH)