ENDOTHELIUM-DEPENDENT CONTRACTIONS TO ACETYLCHOLINE IN THE AORTA OF THE SPONTANEOUSLY HYPERTENSIVE RAT
ENDOTHELIUM-DEPENDENT CONTRACTIONS TO ACETYLCHOLINE IN THE AORTA OF THE SPONTANEOUSLY HYPERTENSIVE RAT
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DOI：
10.1161/01.hyp.8.4.344
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发表时间：
1986-04-01
期刊：
影响因子：
8.3
通讯作者：
VANHOUTTE, PM
中科院分区：
文献类型：
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作者：
LUSCHER, TF;VANHOUTTE, PM
为探讨自发性高血压大鼠（SHR）血管内皮依赖性舒张功能降低的机制，取年龄匹配的雄性SHR和正常血压的Wistar-Kyoto大鼠（WKY）的带内皮和不带内皮的胸主动脉环，进行等长张力记录。乙酰胆碱引起SHR静息环的内皮依赖性收缩，而WKY则无此作用。这些收缩被阿托品抑制，但不是由六烃季铵，并防止磷脂酶A2或环氧合酶的抑制剂，但不是由前列环素合成酶，血栓烷合成酶，或白三烯合成酶的抑制剂。前列腺素D2、E1、E2和F2 α。引起浓度依赖性收缩的环没有内皮细胞从SHR和WKY;的反应，以最高浓度（10-5 M）的个人的alphylandins在两个菌株是可比的。高浓度乙酰胆碱引起的血管内皮依赖性舒张反应在SHR明显低于WKY（p < 0.05），而低浓度乙酰胆碱引起的血管内皮依赖性舒张反应在SHR无显著性差异。吲哚美辛使SHR的内皮依赖性舒张功能正常化。因此，乙酰胆碱可以激活毒蕈碱受体，引起SHR主动脉内皮依赖性收缩，但在WKY主动脉中没有。收缩可能是由环氧化酶产物介导的，而不是前列环素或血栓素A2。SHR对乙酰胆碱的内皮依赖性舒张作用减弱可能不是由于内皮源性舒张因子释放减少，而是由于内皮源性收缩物质同时释放。
To study the mechanism of decreased endothelium-dependent relaxations in spontaneously hypertensive rats (SHR), rings of thoracic aorta with and without endothelium were taken from age-matched male SHR and normotensive Wistar-Kyoto rats (WKY) and suspended for isometric tension recording. Acetylcholine caused endothelium-dependent contractions in quiescent rings from SHR but not in those from WKY. These contractions were inhibited by atropine but not by hexamethonium and were prevented by inhibitors of phospholipase A2 or cyclooxygenase but not by inhibitors of prostacyclin synthetase, thromboxane synthetase, or leukotriene synthetase. Prostaglandin D2, E1, E2, and F2.alpha. caused concentration-dependent contractions in rings without endothelium from both SHR and WKY; the responses to the highest concentration (10-5 M) of the individual prostaglandins were comparable in both strains. Endothelium-dependent relaxations evoked by high but not by low concentrations of acetylcholine were significantly depressed in SHR as compared with those in WKY (p < 0.05). Indomethacin normalized endothelium-dependent relaxations in SHR. Thus, acetylcholine can activate muscarinic receptors that evoke endothelium-dependent contractions in the aorta of SHR but not in that of WKY. The contraction probably is mediated by a cyclooxygenase product(s) other than prostacyclin or thromboxane A2. The reduced endothelium-dependent relaxations to acetycholine in the SHR probably are not due to a decreased release of endothelium-derived relaxing factor(s) but to the simultaneous release of endothelium-derived contracting substance(s).