Artículos de revistas
Perindopril regulates beta-agonist-induced cardiac apoptosis
Fecha
2005-09Registro en:
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY 46(3): 255-261
0160-2446
Autor
Gálvez, A. S.
Fiedler Temer, Jenny
Ocaranza, María Paz
Jalil Milad, Jorge
Lavandero González, Sergio
Díaz Araya, Guillermo
Institución
Resumen
Administration of the P-adrenergic agonist isoproterenol results in cardiac apoptosis. The effect of short-term P-adrenergic stimulation by isoproterenol on the activity of plasma, lung, and left ventricular (LV) angiotensin 1-converting enzyme (ACE) activity and its association with the development of cardiac apoptosis was investigated. P-Adrenergic stimulation for 24 hours produced an early increase only in the proapoptotic proteins bax and bcl-XS without changes in the levels of the antiapoptotic protein bcl-XL. The ratio between these bcl family proteins was indicative of apoptosis and correlated with an early and significant increase (300%) in DNA laddering. However, after 5 days of the P-adrenergic stimulation, the ratio changed in favor of antiapoptotic proteins and correlated with the absence of DNA fragmentation. In addition, LV and plasma ACE activities increased markedly with isoproterenol over the study period up to 5 days. ACE activity also regulated expression of the antiapoptotic gene bcl-XL. The administration of perindopril (an ACE inhibitor) prevented the observed increase in bax and bcl-XS levels and attenuated (50% decrease, P < 0.05) the effect of isoproterenol on DNA fragmentation. Thus, early and transient cardiac apoptosis triggered by the beta-adrenergic agonist isoproterenol is reversed in the presence of perindopril.