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内皮素(endothelin,ET)是两年前才发现的一种强有力的缩血管物质。我们通过离体血管收缩试验观察到,猪内皮素(pET)对人和大鼠的多种血管都有强烈的收缩作用。这种作用较5-羟色胺、去甲肾上腺素、神经肽Y等多种缩血管物质明显而持久,给大鼠注射ET,血压明显升高。家兔实验表明,少至110pg的ET注入颈内动脉即可使脑血流量减少。11ng的ET可以使脑血流量减少80％。局部脑血流量减少的程度和ET剂量相关。给大鼠静脉内注射大剂量ET(32μg/kg),心电图显示心肌缺血、传导阻滞和心脏停搏,大鼠几分钟内死亡。ET的这种心脏毒性可被早期应用降钙素基因相关肽(CGRP)或硝普钠(SNP)所防止。表明ET的心脏毒性可能是通过引起冠状动脉强烈而持久的收缩所致。ET可使血浆醛固酮升高,但抑制下丘脑分泌加压素(AVP)。因此,ET是一个极为重要的血压和血流的调节因子。
Endothelin (ET) is a potent vasoconstrictor that was discovered only two years ago. We showed by an ex vivo vasoconstriction assay that porcine endothelin (pET) has a strong contractile effect on various blood vessels in humans and rats. This effect than serotonin, norepinephrine, neuropeptide Y and other vasoconstrictors obvious and lasting, to rats injected ET, blood pressure was significantly higher. Rabbit experiments show that as little as 110pg of ET injected into the internal carotid artery can reduce cerebral blood flow. 11ng of ET can reduce cerebral blood flow by 80%. The extent of local cerebral blood flow decrease is related to ET dose. Rats were injected intravenously with high-dose ET (32 μg / kg), electrocardiograms showed myocardial ischemia, block and cardiac arrest, and the rats died within a few minutes. This cardiotoxicity of ET can be prevented by early application of calcitonin gene-related peptide (CGRP) or sodium nitroprusside (SNP). Suggesting that the cardiotoxicity of ET may be caused by the strong and lasting coronary artery contraction. ET increases plasma aldosterone but inhibits hypothalamic vasopressin (AVP). Therefore, ET is a very important regulator of blood pressure and blood flow.