REDUCED MITOCHONDRIAL NA+/H+ EXCHANGER 1 PROTEIN EXPRESSION CONTRIBUTES TO THE FUNCTIONAL REMODELING OF THE HYPERTROPHIC RAT HEART MITOCHONDRIA

ÁLVAREZ BV, VARGAS LA.

Boston

Congreso; Experimental Biology 2013; 2013

Mitochondrial dysfunction underlies the causes of numerous cardiac diseases including decompensated cardiac hypertrophy and heart failure. Irreversible opening of the mitochondrial permeability transition pore (MPTP) with the concomitant mitochondrial swelling (MS) characterizes the mitochondrial disturbance. Recently, we revealed the expression of the mitochondrial NHE1 Na+/H+ exchanger (mtNHE1) and demonstrated that inhibition of mtNHE1 protects heart mitochondria from Ca2+-induced MS and MPTP opening. Mitochondria were isolated from normal (NH) and hypertrophic rat hearts (HH), heart weight/body weight ratio 2.8±0.2, and 3.8±0.2, respectively (n=12). MS was measured in mitochondria as a decrease in the light scattering (LS) signal induced by addition of 200 μM CaCl2, and calculated as the difference between LS values before and after addition of Ca2+. The HH mitochondria showed a significant reduction in MS compared to the NH mitochondria, 53±7%, and 100±9%, respectively (n=5, P