Despite the intensive research on hypertension still little data is available about the hypertension-induced changes in cellular bioenergetics as well as in physical and chemical properties of cardiac mitochondria. Aim of the present study is to reveal the effects of untreated hypertension and of anti-hypertensive treatment on the capability of rat cardiac mitochondria to maintain adequate oxidative energy (ATP) production.

Methods: 

Adult male spontaneously hypertensive (SHR) rats (16 week-old) were daily treated for 4 weeks with ACE inhibitor captopril (CAP, 80 mg•kg^-1 p. o.) or with the combination of CAP and the Ca-antagonist nifedipine (NIF, 80 mg•kg^-1 + 10 mg•kg^-1 p. o.). Untreated SHR and similarly old healthy Wistar rats were used as controls. Following parameters were investigated: systolic blood pressure, heart rate, heart to body weight ratio (HW/BW). Subsequently, in isolated cardiac mitochondria membrane fluidity, activity of Mg²⁺-ATPase, rate of oxidative phosphorylation (ROF), ADP:O ratio, O₂ consumption and the content of conjugated dienes were assessed.

Results: 

Mitochondria from SHR hearts exhibited significantly elevated O₂ consumption, ROF, Mg²⁺-ATPase activity and membrane fluidity in response to increased energy demands (all p<0.05). Treatments with CAP and CAP+NIF removed similarly both, hypertension and mitochondrial adaptation by normalizing completely the blood pressure, heart rate and O₂ consumption (all p<0.05) and in part also the ROF, Mg²⁺-ATPase activity and HW/BW. Slight decrease in content of conjugated dienes as compared to the group of healthy Wistar controls was observed in most experimental groups.

Support: Grants VEGA 2/7126/27; 1/0755/09; 2/0173/08 and 1/0142/09.