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说明:关键词: 内皮源性心血管活性物质,一氧化氮(NO),内皮素(ET),血管紧张素Ⅱ(AngⅡ),缓激肽,前列环素(PGI2),腺苷,心血管疾患
内皮源性心血管活性物质是指血管内皮细胞分泌的对心肌收缩力、心率、血管张力等有影响的物质,包括一氧化氮(NO)、内皮素(ET)、血管紧张素Ⅱ(AngⅡ)、缓激肽、前列环素(PGI2)、腺苷等。由于这些物质大多数在局部发挥作用,所以尤以心脏分泌的心血管活性物质更为重要。心脏冠状动脉内皮细胞和心内膜内皮细胞均能分泌心血管活性物质。目前已知内皮分泌的心血管活性物质对心血管系统功能具有重要调节作用,并参与多种心血管疾病的病理生理过程。本文对内皮分泌的心血管活性物质的作用及其与各种心血管疾患的关系等做一综述。
1 一氧化氮(NO)
1.1 来源 NO来源于血管内皮上L-精氨酸的氨基端,在一氧化氮合成酶(NOS)作用下被合成。目前已知有3种一氧化氮合成酶的亚型[1]。第一种亚型称为组成型一氧化氮合成酶(cNOS),主要存在于血管内皮细胞膜上,它发挥作用需钙离子、钙调素、还原型谷胱甘肽(NADPH)等作为辅因子。第二种亚型称为可诱发型(iNOS),主要存在于激活的巨噬细胞中,其发挥作用不需钙离子和钙调素的参与。第三种亚型主要存在于中枢神经系统中。许多生理和化学因素可刺激NO的合成。血流周期性变化使血管内皮上承受的剪切力,是促使NO合成和释放的最重要因素。此外,乙酰胆碱、缓激肽、组胺、P物质、三磷酸腺苷、去甲肾上腺素、中度缺氧等均可使NO释放增加。N-甲基精氨酸通过对NOS的竞争性抑制作用,使NO合成减少。各种氧自由基可迅速清除NO。NO半衰期很短,只有几秒至几十秒。NO从内皮释放后迅速在细胞外液中弥散,并与血管平滑肌上受体结合,使鸟苷酸环化酶激活,环磷酸鸟苷(cGMP)含量增加,从而发挥其生理活性。
目录: 1 一氧化氮(NO)
2 内皮素-1(ET-1)
3 血管紧张素Ⅱ(AngⅡ)
4 缓激肽
5 前列环素(PGI2)
6 腺苷
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