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Dietary supplementation of zinc increases acethylcholine induced relaxations of isolated rat carotid arteries

Objective: Zinc (Zn) and selenium (Se) are important part of antioxidant enzymes which protects against reactive oxygen species (ROS). It has been suggested that altered levels of Zn and/or Se in liver and kidney can contribute or correlate to the impaired antioxidant defense leading to endothelial dysfunction. However, there are few data available regarding the effects of dietary Zn and Se on the vasomotor responses of vessels. Thus we hypothesized that changing dietary content of Zn and Se will alter vasomotor responses of isolated rat carotid arteries. Methods: Male Sprague Dawley rats (n=33) were fed with 4 types of rat chows for 10 weeks: a) low Zn-low Se group (n=8) (normal chow) b) high Zn-high Se (N=5) ; c) high Zn low-Se group (N=10) ; d) low Zn-high Se group (N=10). Carotid arteries (CA) were isolated and their isometric tensions were measured by DMT wire Myograph system. Responses of noradrenaline pre- contracted CA to ACh (10- 9-10-5 M) in the absence or presence of L-NAME. Statistical significance was set at P <0.05 (SigmaPlot v12, Systat Software). Results: Compared to the LSn/LZn (Ach 10-9: -0, 11±0, 03mN, Ach 10-8: -0, 23±0, 04mN, Ach 10-7: -0, 47±0, 07mN, Ach 10-6: -0, 76±0, 11mN, Ach 10-5: -1, 10±0, 16mN, p <0.05) ACh-induced relaxations were significantly greater in LSe/HZn (Ach 10- 9: -0, 36±0, 06mN, Ach 10-8: -0, 63±0, 08mN, Ach 10-7:-1, 15±0, 13mN, Ach 10-6: -1, 68±0, 18mN, Ach 10-5: -2, 02±0, 22mN, p <0.05) and in HSe/HZn(Ach 10-9: -0, 17±0, 10mN, Ach 10-8: -0, 34±0, 13mN, Ach 10-7: -0, 72±0, 18mN, Ach 10-6: -1, 15±0, 23mN, Ach 10-5: -1, 52±0, 24mN, p <0.05) group compared to that of LSe/LZn. Presence of L-NAME blocked ACh- induced vasorelaxation in all four groups of rats. Conclusions: Data suggest: 1) changes in dietary Zn and Se substantially affects arterial relaxations to ACh, 2) presence of high level of Zn is responsible for the improved endothelial function and 3) the underlying mechanisms likely include increased NO bioavailability.

zinc; carotid arteries; actylcholine; rats

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