Biochemical mechanisms of the energy-protective action of blockers of slow high-threshold L-type calcium channels

This review discusses information about the structure and function of calcium channels in plasma membrane mitochondria heart, pharmacological methods for modulating their conductance. Experimental data are presented that characterize change energy metabolism cardiomyocytes against background transformation conductivity L-type cell a non-invasive model vibration-mediated (56 sessions total vertical vibration, with frequency 44 Hz an amplitude 0.5 mm) hypoxia.
 It was shown animals treated channel blocker adalat (nifedipine INN) rate endogenous respiration (Ve), measured by polarographic method using closed Clark electrode native homogenate rabbit myocardial tissue, remained at level intact amounted to 16.3 4.3 ng-O atom/ min mg protein, amytal sensitivity increased 39% (p 0.05) compared group vibrated animals, low-natality decreased 40% 0.05). The dynamics substrate (Vac Vglu + mal) returned which indicated restoration physiological predominance activity theNADH CoQ-reductase complex redox reactions. found blockade transport Ca2+ ions high-threshold (HVA) voltage-dependent ion membrane, normalizing I enzyme-substrate respiratory chain regulatoryly restraining hyperactivity succinate dehydrogenase zone II complex, has energy-protective effect. Adalat prevented low-energy shift development bioenergetic hypoxia tissue experimental animals.