PROTEíNAS Y CORRIENTES EN CANALES DE SODIO

ITUARTE L; VIERA B; ZANETTI MN; SARAVÍ F; SALDEÑA T

San Juan

Congreso; 2da Reunión Conjunta de Sociedades de Biología de la República Argentina; 2011

SOCIEDAD ARGENTINA DE BIOLOGÍA

Hypoxia increases cardiac action potential duration and may predispose to lethal arrhythmias. Low oxygen pressure (hypobaric hypoxia) augments potential-dependent Na currents (INa) and this effect may be clinically relevant as an arrhythmia-triggering mechanism. This work aimed at obtaining a mathematical function for the relationship between INa and membrane potential based on experimental results and to assess changes in protein expression caused by hypoxia. Rats were exposed to either normal pressure or chronic hypobaric hypoxia. Isolated myocytes were obtained and INa was measured in them under potential clamp conditions before and after applying tetrodotoxin. Tetrodotoxin-sensitive INa was significantly higher in cells from hypoxic rats. With a function linearization method, the mathematical function was y= 598 . x . 10 0.01 x for controls and y = 1257.x.10 0.01x for chronic hypoxia. These theoretical functions obtained from experimental results allow calculating INa for a given transmembrane potential. Protein expression analysis was carried out with 12 % polyacrylamide gel electrophoresis in homogenates obtained from myocytes of both groups. It was found that chronic hypoxia caused a dramatic change in protein expression. The different values calculated for the constant term of the mathematical function for the relationship between potential difference and INa in each group are related to the INa increase induced by chronic hypoxia, which in turn may be caused by changes in protein expression, although further work is needed to adequately characterize those changes.