INDIRECT EVIDENCE FOR AN ENDOTHELIUM-DERIVED CONTRACTING FACTOR RELEASE IN AORTA OF DEOXYCORTICOSTERONE ACETATE-SALT HYPERTENSIVE RATS
INDIRECT EVIDENCE FOR AN ENDOTHELIUM-DERIVED CONTRACTING FACTOR RELEASE IN AORTA OF DEOXYCORTICOSTERONE ACETATE-SALT HYPERTENSIVE RATS
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DOI：
10.1097/00004872-199001000-00009
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发表时间：
1990-01-01
影响因子：
4.9
通讯作者：
NIGRO, D
中科院分区：
文献类型：
--
作者：
CORDELLINI, S;CARVALHO, MHC;NIGRO, D
为了探讨内皮源性血管活性物质在醋酸脱氧皮质酮（DOCA）盐性高血压中的作用，研究了在吲哚美辛不存在和不存在的情况下，去甲肾上腺素、乙酰胆碱、硝普钠和罂粟碱的反应。去甲肾上腺素对doca盐高血压大鼠有内皮或无内皮的主动脉收缩反应同样有效，而在对照组中，去甲肾上腺素摩擦组比未摩擦组诱导更高的次极大反应。用去甲肾上腺素预收缩内皮的高血压大鼠主动脉对内皮依赖性血管扩张剂乙酰胆碱的反应降低。对照组和doca盐高血压组在去内皮后松弛反应消失。在高血压大鼠分离的主动脉中，硝普钠（一种不依赖内皮的药物）的反应和罂粟碱（一种部分依赖内皮的药物）的反应没有改变。吲哚美辛治疗仅改变未摩擦高血压大鼠主动脉对去甲肾上腺素的反应。在这些制剂中，观察到对去甲肾上腺素的双相反应。在较低浓度下，去甲肾上腺素诱导特征性收缩反应，而在较高浓度下，获得松弛反应，被鸟苷酸环化酶抑制剂亚甲基蓝所消除。提示去甲肾上腺素可诱导高血压大鼠主动脉内皮源性松弛因子（EDRF）的释放。此外，吲哚美辛治疗可以恢复doca盐高血压大鼠主动脉对乙酰胆碱的反应。这表明，doca盐高血压导致主动脉对乙酰胆碱的反应受损，对去甲肾上腺素的反应增加，这是因为一些内皮细胞功能的改变，这与EDRF的释放和/或产生减少无关，而是与内皮源性收缩因子（EDCF）的同时释放有关，该因子对吲哚美辛酸阻断敏感。
In order to investigate the involvement of endothelium-derived vasoactive substances in deoxycorticosterone acetate (DOCA)-salt hypertension, the responses to noradrenaline, acetylcholine, sodium nitroprusside and papaverine were studied in the absence and presence of indomethacin. Noradrenaline was equally effective in evoking a constrictor response of aorta, with or without endothelium, isolated from DOCA-salt hypertensive rats, while in controls, noradrenaline induced higher submaximal responses in rubbed than in unrubbed preparations. A decreased response to acetylcholine, an endothelium-dependent vasodilator, was observed in aorta with endothelium which had been precontracted with noradrenaline isolated from hypertensive rats. The relaxant response was lost after removal of the endothelium in both control and DOCA-salt hypertensive groups. The response to sodium nitroprusside, an endothelium-independent agent, in aorta isolated from hypertensive rats as well as the response to papaverine, an agent partially dependent on the endothelium, was not altered. Indomethacin treatment altered the response to noradrenaline only in unrubbed aorta of hypertensive rats. In these preparations, a biphasic response to noradrenaline was observed. At lower concentrations noradrenaline induced the characteristic constrictor response, while at higher concentrations a relaxant response was obtained that was abolished by methylene blue, a guanylate cyclase inhibitor. This could indicate that noradrenaline induced the release of endothelium-derived relaxing factor (EDRF) in aorta of hypertensive rats. Furthermore, indomethacin treatment restored the decreased response to acetylcholine in aorta isolated from DOCA-salt hypertensive rats. It is suggested that DOCA-salt hypertension causes an impaired response to acetylcholine and an increased response to noradrenaline in aorta because of an alteration of some endothelial cell function which is not related to a diminished release and/or production of EDRF, but to a simultaneous release of an endothelium-derived contracting factor (EDCF) which is sensitive to indomethacin blockade.