Experimental Physiology - Symposium Report Role of nitric oxide and prostacyclin as vasoactive hormones released by the endothelium
Experimental Physiology - Symposium Report Role of nitric oxide and prostacyclin as vasoactive hormones released by the endothelium
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发表时间：
2007
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通讯作者：
Jane A. Mitchell;F. Ali;Lucy K. Bailey;L. Moreno;L. S. Harrington
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作者：
Jane A. Mitchell;F. Ali;Lucy K. Bailey;L. Moreno;L. S. Harrington
内皮细胞排列在每根血管的管腔表面，使其与循环血液元素以及下面的血管平滑肌层接触。在健康血管中，内皮表达一氧化氮合酶（NOSIII）和环加氧酶（COX-1）的组成形式，它们分别产生血管活性激素NO和前列环素。一氧化氮和前列环素均能放松血管，抑制血小板活化。前列环素的作用是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激活受体(PPAR)β介导的。NO的作用主要通过激活细胞内的鸟苷环化酶介导，导致cGMP的形成。在血小板中，一氧化氮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，诱导形式的NOS （NOSII）和环氧酶（COX-2）在血管平滑肌中表达，导致大量NO、前列环素和前列腺素E2的释放。NOSII和COX-2在血管炎症中的相对作用仍有争议，但可能导致保护性和破坏性反应。本文讨论了NOS和COX组成形式的相对贡献，以及血管和血小板中IP、PPARβ和guanyyl环化酶途径之间的相互作用。
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)β. 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 E2. 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, PPARβ and guanylyl cyclase pathways in vessels and platelets, is discussed.