Journal
VASCULAR PHARMACOLOGY
Volume 58, Issue 1-2, Pages 64-70Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.vph.2012.07.005
Keywords
Resveratrol; Vasorelaxation; Calcium influx; Calcium release; Abdominal aorta
Categories
Funding
- National Natural Science Foundation of China [30971060, 30900535]
- Shaanxi Province [2010K01195, S2011JC5080]
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Evidence has indicated that resveratrol (Res) produces vasorelaxation and may decrease the coronary heart disease mortality. However, several pathways involved in the mechanism of vasorelaxation are still unclear. This study was designed, therefore, to test the probable ion channels or receptors involved in the mechanism. The abdominal aortic rings from the male Sprague-Dawley rats were perfused in the organ chambers filled with Kreb's solution, where the tension of each ring was measured. Treatment with L-NAME (a nitric oxide synthase inhibitor), glibenclamide and tetraethylammonium (TEA) significantly attenuated the vasorelaxing effect of Res. In lower concentration Res relaxed the ring in an endothelium-dependent manner, while in higher concentration the endothelium-independent manner could be observed. In calcium-free Kreb's solution, Res inhibited vasoconstriction induced by NE. With intracellular calcium depleted by thapsigargin, Res also inhibited vasoconstriction induced by Kreb's solution with high potassium via L-Ca2+ channel. In a word, Res decreased both extracellular calcium influx and intracellular calcium release. These results suggest that: (1) Res may exert its relaxing effect on abdominal aorta by opening K+ channel to hyperpolarize vascular smooth muscle.(2) Res relaxes the abdominal aorta in both endothelium-dependent and endothelium-independent manners. (3) Finally, Res attenuates both extracellular calcium influx and intracellular calcium release, which results in vasorelaxation. (C) 2012 Elsevier Inc. All rights reserved.
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