The Na+/HCO3- co-transporter and the carbonic anhydrase contribute to myocardial reperfusion injury

FANTINELLI JC; ,A ORLOWSKI; ALVAREZ BERNARDO VICTOR; A AIELLO; MOSCA SM

Foz de Iguazu

Congreso; 1º Panamericann Congress of Physiological Sciences; 2014

The HCO3 - is the main buffer and primary waste product of cellular metabolism. Cells control the HCO3 - movement through plasma membrane by the activity of exchanger Cl-/HCO3 - and the Na+/HCO3 - co-transporter (NBC). In the heart have been described at least three isoforms of NBC: an electroneutral (NBCn) and two electrogenic isoforms (NBCe, 1Na+:2HCO3 -). During ischemia-reperfusion NBC activate contributing to the increase of intracellular Na+ and secondarily to Ca2+ overload. The increase of intracellular Ca2+ is one of the factors responsible for the reperfusion injury. Recently, in our laboratory, functional antibodies against extracellular loops 3 (a-L3) and 4 (a-L4) of NBCe were synthesized. Additionally, it has been demonstrated that NBC physically and functionally interact with the carbonic anhydrase (CA) forming ion transport metabolon. However, the participation of NBCe and CA in ischemia-reperfusion is not fully elucidated. To assess the contribution of Na+/HCO3 - cotransporter electrogenic isoform (NBCe1) and carbonic anhydrase (CA) to infarct size and myocardial dysfunction caused by ischemiareperfusion in isolated rat heart.These data show that NBCe1 and CA contribute to the infarct size generation and myocardial dysfunction produced by ischemia-reperfusion in isolated rat heart. Therefore, the blockade of both entities exerts a cardioprotective effect which could be attributed to the reduction of Ca2+ overload.