Role of nitric oxide and prostacyclin as vasoactive hormones released by the endothelium
Role of nitric oxide and prostacyclin as vasoactive hormones released by the endothelium
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DOI：
10.1113/expphysiol.2007.038588
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发表时间：
2008-01-01
影响因子：
2.7
通讯作者：
Harrington, Louise S.
中科院分区：
文献类型：
--
作者：
Mitchell, Jane A.;Ali, Ferhana;Harrington, Louise S.
内皮排列在每个血管的管腔表面，使其与循环血液成分以及下面的血管平滑肌层接触。在健康血管中，内皮表达组成型一氧化氮合酶（NOSIII）和环氧合酶（考克斯-1），其分别产生血管活性激素NO和前列环素。NO和前列环素都能舒张血管，抑制血小板活化。前列环素的作用由细胞表面前列环素（IP）受体和/或细胞内过氧化物酶体增殖物激活受体（PPAR）β介导。NO的作用主要通过细胞内鸟苷酸环化酶的活化介导，导致cGMP的形成。在血小板中，NO和前列环素的作用是协同的，但在血管中，它们的作用是相加的。在病变血管中，诱导型NOS（NOS II）和环氧合酶（考克斯-2）在血管平滑肌中表达，导致大量NO、前列环素和前列腺素E-2的释放。NOSII和考克斯-2对血管炎症的相对贡献仍有争议，但可能导致保护性和损伤性反应。NOS和考克斯的组成形式的相对贡献，以及IP，PPAR β和鸟苷酸环化酶途径在血管和血小板之间的相互作用，进行了讨论。
The endothelium lines the luminal surface of every blood vessel, allowing it contact with circulating blood elements, as well as the underlying vascular smooth muscle layer. In healthy vessels, the endothelium expresses constitutive forms of nitric oxide synthase (NOSIII) and cyclo-oxygenase (COX-1), which produce the vasoactive hormones NO and prostacyclin, respectively. Both NO and prostacyclin relax blood vessels and inhibit platelet activation. The actions of prostacyclin are mediated by cell surface prostacyclin (IP) receptors and/or intracellular peroxisome proliferator-activated receptors (PPAR)beta. The actions of NO are mediated predominately by activation of intracellular guanylyl cyclase, leading to the formation of cGMP. In platelets, the actions of NO and prostacyclin are synergistic, but in vessels their actions are additive. In diseased vessels, inducible forms of NOS (NOSII) and cyclo-oxygeanse (COX-2) are expressed in vascular smooth muscle, resulting in the release of large amounts of NO, prostacyclin and prostaglandin E-2. The relative contribution of NOSII and COX-2 to vascular inflammation is still debated, but is likely to result in both protective and damaging responses. The relative contribution of constitutive forms of NOS and COX, as well as interactions between IP, PPAR beta and guanylyl cyclase pathways in vessels and platelets, is discussed.