摘要
目的 探讨自发性高血压大鼠 (SHR)内皮舒张功能不全的发生机制。方法 采用体外灌注的方法测定大鼠胸主动脉环对不同浓度乙酰胆碱的舒张反应变化 ,并测定血清中NO-3浓度和动脉组织中环鸟苷酸水平。结果 与魏 凯二氏大鼠 (WKY)比较 ,SHR胸主动脉环对乙酰胆碱的舒张反应明显减弱。左旋硝基精氨酸 (L NNA)可明显抑制大鼠胸主动脉环对乙酰胆碱的舒张反应 ,但并不能消除SHR和WKY对乙酰胆碱舒张反应之间的差异。与WKY比较 ,SHR血中NO-3水平明显降低 (P<0 .0 1) ,动脉组织中环鸟苷酸含量降低 (P<0 .0 1)。结论 SHR内皮依赖的血管舒张功能减低 ;一氧化氮 (NO)的生成或释放不足可能直接参与了SHR血管内皮依赖的舒张功能不全。
Objective Vascular endothelial cells play an important role in the regulation of vascular wall by producing vasoactive agents,such as nitric oxide (NO),angiotensin Ⅱ (AⅡ) etc.The goal of the present study was to investigate the changes of NO pathway in vascular endothelium of spontaneously hypertensive rat (SHR).Methods The animals aged 17 months were divided into two groups: SHRs(n=10)and WKY rats(n=10).Blood pressure was messured by the tail cuff method .To study the endothelium dependent relaxation in response to Ach,rings of thoracic aorta with and without endothelium were taken from SHR and WKY rats and suspended in organ chambers,which contained 10 ml K H solution(37℃) aerated with 95% O 2 and 5% CO 2 and connected to force transducers for isometric tension recording.NO - 3concentration in serum was assayed by activated cadmium reduction method; cGMP levels in vascular tissue were assayed by RIA.Results The rings of thoracic aorta without endothelium had no response to Ach in either SHRs or WKY rats.In SHR,endothelium dependent relaxation of the rings with endothelium evoked by Ach was significantly depressed as compared with that in WKY rats.In all rings with endothelium,the Ach induced relaxation was markedly prevented by 10 -3 mmol/L of L nitroarginine (L NNA).Compared with WKY rats,blood NO - 3 concentration and vascular cGMP level were reduced in SHR.Conclusions The results indicate that the endothelium dependent vascular relaxation is attenuated in SHR,possibly by diminished synthesis or release of NO.
出处
《中华老年心脑血管病杂志》
CAS
2000年第1期41-44,共4页
Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
关键词
自发性高血压大鼠
一氧化氮
内皮功能不全
spontaneously hypertensive rat
nitric oxide
endothelial dysfunction