ИСТИНА

This study examined whether coenzyme Q10 can improve NO dependent vasodilatation in the rat aorta after pre-incubation or intravenous administration. In initial experiments, intact isolated aortic rings were incubated with CoQ10 or L-arginine. In further experiments, CoQ10 was administered intravenously in anesthetized rats, and then in 2 hours, aorta was isolated. In both cases, after preliminary preparation the isolated aortic rings were tested for Ach induced NO dependent relaxation. ACh elicited a concentration dependent relaxation of phenylephrine pre-contracted aortic rings. Relaxant responses to ACh were markedly potentiated after pre-incubation with CoQ10 or L-arginine. The maximum relaxant responses (%) were significantly increased from 64.1±5.3 (control) to 89.8±3.0 and 83.6±3.0 (CoQ10 and L-arg, respectively). The pD2 (-lgEC50) value in control study was 5.81±0.28, after pre-treatment with CoQ10 or L-arg were 7.59±0.16 and 7.26±0.32, respectively. There was no difference between CoQ10 and L-arginine groups. After intravenous administration, the relaxant responses to ACh were significantly increased in CoQ10-treated group (94.2±2.0) compared with controls (68.1±4.4). pD2 values were also different between control and treatment groups (5.79±0.29 vs. 8.14±0.65, respectively). Thus, CoQ10 improved NO mediated vasodilation in rat aorta as well as substrate for eNOS-L-arginine. Our data show that exogenous intravenously administered CoQ10 is able to improve rapidly NO dependent vasodilation in rat aorta, likely due to accumulation of CoQ10 in the vessel wall. Improvement of endothelial function can contribute, at least in part, to beneficial effects of CoQ10 in cardiovascular diseases associated with endothelial dysfunction.