Effect of antihypertensive agents - captopril and nifedipine - on the functional properties of rat heart mitochondria | ||
| Iranian Journal of Basic Medical Sciences | ||
| مقاله 6، دوره 19، شماره 6، شهریور 2016، صفحه 615-623 اصل مقاله (1007.88 K) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2016.7129 | ||
| نویسندگان | ||
| Ivana Kancirová1؛ Magdaléna Jašová1؛ Iveta Waczulíková2؛ Táňa Ravingerová3؛ Attila Ziegelhöffer1؛ Miroslav Ferko* 1 | ||
| 1Department of Biochemistry, Institute for Heart Research, Centre of Excellence SAS NOREG, Slovak Academy of Sciences, Bratislava, Slovakia | ||
| 2Department of Nuclear Physics and Biophysics, Faculty of Mathematics, Physics, and Informatics, Comenius University, Bratislava, Slovakia | ||
| 3Department of Physiology, Institute for Heart Research, Centre of Excellence SAS NOREG, Slovak Academy of Sciences, Bratislava, Slovakia | ||
| چکیده | ||
| Objective(s): Investigation of acute effect on cellular bioenergetics provides the opportunity to characterize the possible adverse effects of drugs more comprehensively. This study aimed to investigate the changes in biochemical and biophysical properties of heart mitochondria induced by captopril and nifedipine antihypertensive treatment. Materials and Methods: Male, 12-week-old Wistar rats in two experimental models (in vivo and in vitro) were used. In four groups, the effects of escalating doses of captopril, nifedipine and combination of captopril + nifedipine added to the incubation medium (in vitro) or administered per os to rat (in vivo) on mitochondrial ATP synthase activity and membrane fluidity were monitored. Results: In the in vitro model we observed a significant inhibitory effect of treatment on the ATP synthase activity (P<0.05) with nonsignificant differences in membrane fluidity. Decrease in the value of maximum reaction rate Vmax(P<0.05) without any change in the value of Michaelis-Menten constant Km, indicative of a noncompetitive inhibition, was presented. At the in vivo level, we did not demonstrate any significant changes in the ATP synthase activity and the membrane fluidity in rats receiving captopril, nifedipine, and combined therapy. Conclusion: In vitro kinetics study revealed that antihypertensive drugs (captopril and nifedipine) directly interact with mitochondrial ATP synthase. In vivo experiment did not prove any acute effect on myocardial bioenergetics and suggest that drugs do not enter cardiomyocyte and have no direct effect on mitochondria. | ||
| کلیدواژهها | ||
| Captopril؛ Heart؛ Membrane fluidity؛ Mitochondria؛ Mitochondrial proton-translocating ATPases؛ Nifedipine | ||
| مراجع | ||
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