Abstract

This study examined whether coenzyme Q10 can improve nitric oxide (NO)-dependent vasodilatation in the rat aorta after pre-incubation or intravenous administration. In initial experiments, intact isolated aortic rings were incubated with coenzyme Q10 or L-arginine. In further experiments, coenzyme Q10 was administered intravenously in anesthetized rats, then in 2h aorta was isolated. In both cases, after preliminary preparation the isolated aortic rings were tested for acetylcholine-induced NO-dependent relaxation. Acetylcholine elicited concentration-dependent relaxation of phenylephine precontracted aortic rings. Relaxant responses to acetylcholine were markedly potentiated after pre-incubation with coenzyme Q10 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 (coenzyme Q10 and L-arginine, respectively). pD2 (-lgEC50) value in control study was 5.81±0.28, after pretreatment with coenzyme Q10 or L-arginine were 7.59±0.16 and 7.26±0.32, respectively. There was no difference between coenzyme Q10 and L-arginine groups. After intravenous administration, the relaxant responses to acetylcholine were significantly increased in coenzyme Q10-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, coenzyme Q10 improved NO-mediated vasodilation in rat aorta in magnitude close to the effects of L-arginine - substrate for eNOS. Our data first show that exogenous coenzyme Q10 through intravenous administration is able to improve rapidly NO-dependent vasodilation in rat aorta, likely due to accumulation of coenzyme Q10 in the vessel wall. Improvement of endothelial function can contribute, at least in part, to beneficial effects of coenzyme Q10 in cardiovascular diseases associated with endothelial dysfunction.

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