Beneficial effect of coenzyme Q injection on nitric oxide -related dilation of the rat aorta.

This study examined whether coenzyme Q 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 Q or L-arginine. In further experiments, coenzyme Q 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 Q 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 Q and L-arginine, respectively). pD (-lgEC) value in control study was 5.81±0.28, after pretreatment with coenzyme Q or L-arginine were 7.59±0.16 and 7.26±0.32, respectively. There was no difference between coenzyme Q and L-arginine groups. After intravenous administration, the relaxant responses to acetylcholine were significantly increased in coenzyme Q-treated group (94.2±2.0) compared with controls (68.1±4.4). pD values were also different between control and treatment groups (5.79±0.29 vs. 8.14±0.65, respectively). Thus, coenzyme Q 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 Q through intravenous administration is able to improve rapidly NO-dependent vasodilation in rat aorta, likely due to accumulation of coenzyme Q in the vessel wall. Improvement of endothelial function can contribute, at least in part, to beneficial effects of coenzyme Q in cardiovascular diseases associated with endothelial dysfunction.