Ain Baroreflex dysfunction is associated with a higher rate of sudden death after myocardial infarction(MI).Ketanserin enhances baroreflex function in rats.The present work was designed to examine whether ketanserin improves the postMI cardiac function and to explore the possible mechanism involved.Methods Spontaneously hypertensive rats (SHR) were treated with ketanserin (0.3 mg · kg1 · d1).Two weeks later, blood pressure and baroreflex function were measured, followed by a ligation of the left coronary artery.The expressions of vesicular acetylcholine transporter (VAChT) and α7 nicotinic acetylcholine receptor (α7nAChR) in ischemic myocardium, angiogenesis, cardiac function, and left ventricular (LV) remodeling were evaluated subsequently.Resuits Ketanserin significantly improved baroreflex sensitivity (0.62 ± 0.21 vs.0.34 ± 0.12 ms/mmHg, P <0.01) and vagal tonic activity (heart rate changes in response to atropine, 54.8 ± 16.2 vs.37.6 ± 13.4 b.p.m.,P < 0.01) without affecting the blood pressure or basic heart rate in SHR.Treatment of SHR with ketanserin prominently improved cardiac function and alleviated LV remodeling, as reflected by increases in the ejection fraction,fractional shortening, and LV systolic pressure as well as decreases in LV internal diameter and LV relative weight.The capillary density, vascular endothelial growth factor expression, and blood flow in the ischemic myocardium were significantly higher in the ketanserintreated group.In addition, ketanserin markedly increased the expression of VAChT and α7nAChR in ischemic myocardium.Conclusion Ketanserin improved postMI cardiac function and angiogenesis in ischemic myocardium.The findings provide a mechanistic basis for restoring baroreflex function using ketanserin in the treatment of MI.