CENTRO DE INVESTIGACIONES CARDIOVASCULARES "DR. HORACIO EUGENIO CINGOLANI"
Unidad Ejecutora - UE
congresos y reuniones científicas
Regulation of the cardiac soidum/bicarbonate cotransport by angiotensin II, reactive oxygen species and elevated carbon dioxide.
Conferencia; VIII International Congress of the Society for Free Radical Biology and Medicine.; 2013
Regulation of the cardiac sodium/bicarbonate cotransport by angiotensin II, reactive oxygen species and elevated carbon dioxide. Aiello EA. Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas, UNLP-CONICET, La Plata, Argentina. The sodium/bicarbonate cotransporter (NBC) is, with the Na+/H+ exchanger (NHE), an important alkalinizing mechanism that maintains cellular intracellular pH (pHi). In the heart exists at least two isoforms of NBC, one that promotes the co-influx of 1 molecule of Na+ per 1molecule of HCO3- (electroneutral isoform; nNBC) and one that generates the co-influx of 1 molecule of Na+ per 2 molecules of HCO3- (electrogenic isoform; eNBC). We demonstrated that eNBC generates an anionic repolarizing current that modulate the cardiac action potential, adding to such isoform the relevance to modulate the electrophysiological function of the heart. On the other hand, we have recently reported that cell exposure to elevated CO2 concentration upregulates the function and expression of nNBC, reflecting augmented cellular capacity for counteracting intracellular acidosis inflicted by high CO2. Angiotensin II (Ang II) is one of the main hormones that regulate cardiac physiology. Interestingly, we have shown that Ang II exhibits an opposite effect on NBC isoforms: it activates the nNBC through the production of reactive oxygen species (ROS) and the stimulation of the ERK MAPKinase and inhibits the eNBC through the activation of the p38 MAPkinase. The regulation of the intracellular Na+ concentration and pHi is crucial for the cardiac cellular physiology, but these ions are also involved in the development of cardiac hypertrophy and the damage produced by ischemia-reperfusion, suggesting a potential role of NBC in cardiac diseases.