Baroreflex deficiency hampers angiogenesis after myocardial infarction via acetylcholine-α7-nicotinic ACh receptor in rats.

摘要: Aims Angiogenesis is critical for re-establishing blood supply to ischaemic myocardium after myocardial infarction (MI). Human studies have associated arterial baroreflex (ABR) deficiency with higher rate of sudden death MI. The present work was designed examine whether ABR affects angiogenesis in MI rats. Methods and results Baroreflex sensitivity (BRS) determined conscious rats at 1 month occlusion the left anterior descending coronary artery. survival time significantly shorter Sprague-Dawley BRS <0.60 ms/mmHg vs. those ≥0.60 ms/mmHg. Sinoaortic denervation destroyed ABR, decreased capillary density, regional flow vascular endothelial growth factor (VEGF) concentration Ketanserin (0.6 mg/kg/day) enhanced BRS, increased flow, VEGF. also reduced expression vesicular acetylcholine (ACh) transporter α7-nicotinic ACh receptor (α7-nAChR). attenuated α7-nAChR knockout mice. In contrast, increase endogenous cholinesterase inhibitor pyridostigmine (30 cultured cardiac microvascular cells, stimulated VEGF, phosphorylation VEGF 2, tube formation a manner dependent upon α7-nAChR. Conclusion Our demonstrated that could attenuate myocardium. These findings provide further mechanistic basis enhancing function treatment