Mitochondrial Membrane Potential and Oxygen Consumption in Spontaneously Hypertensive Rats

Hypertension is characterized by non-effective cardiac performance but the mechanisms remain unknown. In studies on spontaneously hypertensive rats (SHR) and Wistar rats, we evaluated the effectiveness of the cardiac mitochondria functioning by comparing the levels of mitochondrial membrane potential, respiration and oxidative phosphorylation. Measurement of mitochondrial membrane potential in suspensions of heart mitochondria was performed using a TPMP+-selective electrode following the method described by M.Brand. Mitochondrial oxygen consumption and oxidative phosphorylation were investigated using the device "Oxygraph." Membrane potential of SHR cardiac mitochondria has been revealed as -113.76 mV ± 3.65 mV, that was significantly lower than in control whereas the rate of oxygen consumption in both a state of relative rest (V2), and the active state (V3) was significantly increased (P < 0.001). At the same time respiratory control of SHR cardiac mitochondria was decreased by 23.9% (P < 0.05), which reflects the degree of coupling of substrate oxidation and ADP phosphorylation. The obtained results indicate more intensive work of respiratory chain and a reduced energy-producing function of cardiac mitochondria in animals with genetically determined hypertension. Thus, impaired functional state of mitochondria and lowered energy supply may underlie the myocardium dysfunction in arterial hypertension.