PROSTAGLANDIN-H2 MAY BE THE ENDOTHELIUM-DERIVED CONTRACTING FACTOR RELEASED BY ACETYLCHOLINE IN THE AORTA OF THE RAT
PROSTAGLANDIN-H2 MAY BE THE ENDOTHELIUM-DERIVED CONTRACTING FACTOR RELEASED BY ACETYLCHOLINE IN THE AORTA OF THE RAT
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DOI：
10.1161/01.hyp.15.5.475
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发表时间：
1990-05-01
期刊：
影响因子：
8.3
通讯作者：
SATAKE, T
中科院分区：
文献类型：
--
作者：
KATO, T;IWAMA, Y;SATAKE, T
本实验旨在鉴定乙酰胆碱刺激自发性高血压大鼠（SHR）和正常Wistar-Kyoto大鼠（WKY）主动脉产生的内皮源性收缩因子。取年龄匹配的SHR和WKY大鼠的胸主动脉环，记录其等长张力的变化。SHR大鼠主动脉环对乙酰胆碱的松弛反应明显弱于WKY大鼠。经环氧化酶抑制剂（吲哚美辛）或血栓素A2/前列腺素H2受体拮抗剂（ONO-3708）预处理后，SHR和WKY大鼠主动脉环对乙酰胆碱的松弛反应均显著增强。一种血栓素A2合成酶抑制剂（OKY-046）不影响SHR或WKY大鼠的乙酰胆碱诱导的主动脉环松弛。在器官浴液中，乙酰胆碱刺激后，前列腺素E2和6-酮-前列腺素f1 . α。前列腺素f2 - α浓度升高，但不升高。血栓素B2浓度。外源性前列腺素H2，血栓素A2的稳定类似物，和前列腺素f2。较低浓度的前列腺素E2、前列腺素D2和前列腺素I2诱导SHR环收缩。这些对各种前列腺素的收缩反应被ONO-3708预处理明显抑制。前列环素合成酶抑制剂不影响SHR环对乙酰胆碱的松弛反应。这些结果表明，乙酰胆碱刺激不仅在SHR大鼠的主动脉中产生并释放内皮源性收缩因子，而且在WKY大鼠的主动脉中也能产生和释放内皮源性收缩因子，提示释放的前列腺素的前体前列腺素H2是乙酰胆碱刺激产生的内皮源性收缩因子的有力候选物。
The present experiment was performed to identify endothelium-derived contracting factor produced by acetylcholine stimulation in the aorta of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. The rings of the thoracic aorta were obtained from age-matched SHR and WKY rats, and changes in isometric tension were recorded. The relaxant responses to acetylcholine in the aortic rings from SHR were significantly weaker than those from WKY rats. The relaxant responses to acetylcholine were significantly enhanced by pretreatment with a cyclooxygenase inhibitor (indomethacin) or thromboxane A2/prostaglandin H2 receptor antagonist (ONO-3708) in aortic rings from both SHR and WKY rats. A thromboxane A2 synthetase inhibitor (OKY-046) did not affect the acetylcholine induced relaxation in the aortic rings from SHR or WKY rats. In the organ bath solution, after acetylcholine stimulation, prostaglandin E2 and 6-keto-prostaglandin F1.alpha. concentrations increased but not prostaglandin F2.alpha. and thromboxane B2 concentrations. Exogenous prostaglandin H2, a stable analogue of thromboxane A2, and prostaglandin F2.alpha. induced contractions of the SHR rings at a lower concentration than prostaglandin E2, prostaglandin D2, and prostaglandin I2. These contractile responses to various prostaglandins were markedly inhibited by pretreatment with ONO-3708. A prostacyclin synthetase inhibitor did not affect the relaxant responses to acetylcholine in the SHR rings. These results show that endothelium-derived contracting factor is produced and released by acetylcholine stimulation not only in the aorta of SHR but also in those of WKY rats and suggest that prostaglandin H2, a precursor of the released prostaglandins, is a strong candidate for endothelium-derived contracting factor produced by acetylcholine stimulation.