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However, little information is available on the metabolic pattern and arteriogenesis of VSMCs after MI. VNS has been shown to stimulate the expression of CPT1\u03b1, CPT1\u03b2, Glut1, Glut4 and SDF-1\u03b1 in coronary VSMCs, decreasing the number of CD68-positive macrophages while increasing CD206-positive macrophages in the infarcted hearts, leading to a decrease in TNF-\u03b1 and IL-1\u03b2 accompanied by a reduced ratio of CD68- and CD206-positive cells, which were dramatically abolished by atropine and mecamylamine in vivo. Knockdown of SDF-1\u03b1 substantially abrogated the effect of VNS on macrophagecell alteration and inflammatory factors in infarcted hearts. Mechanistically, ACh induced SDF-1\u03b1 expression in VSMCs in a dose-dependent manner. Conversely, atropine, mecamylamine, and a PI3K\/Akt inhibitor completely eliminated the effect of ACh on SDF-1\u03b1 expression. 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