Lüscher T F, Richard V, Tschudi M, Yang Z
Department of Medicine, University Hospital, Basel, Switzerland.
Clin Physiol Biochem. 1990;8 Suppl 3:108-19.
Serotonin has many and opposing effects in the cardiovascular system. The vascular endothelium importantly contributes as a modulator and mediator of the cardiovascular effects of serotonin. Endothelial cells contain the enzyme monoaminooxidase which inactivates serotonin. In addition, endothelial cells are a source of vasodilator substances such as endothelium-derived relaxing factor, the endogenous nitrovasodilator. Nitric oxide is continuously formed by the arterial endothelium to inhibit the effects of vasoconstrictor substances such as serotonin. Accordingly, removal of the endothelium enhances contractions induced by serotonin in most vascular preparations. In certain blood vessels, such as the porcine and canine coronary artery, serotonin stimulates the release of endothelium-derived nitric oxide. Endothelium-dependent relaxations to serotonin also occur in intramyocardial porcine coronary resistance arteries. In contrast to porcine and canine arteries, endothelium-dependent relaxations to serotonin have not been demonstrated in the human coronary and internal mammary artery. In the porcine coronary artery with regenerated endothelium and in that with atherosclerotic changes, the endothelium facilitates contractions to serotonin, suggesting that an endothelium-derived contracting factor is released. Since indomethacin prevents this endothelium-dependent facilitation of contractions to serotonin in atherosclerotic porcine coronary arteries, a cyclooxygenase product is likely involved. Similarly, in the aorta of spontaneously hypertensive rats, the endothelium facilitates the contractions to serotonin. Thus, the endothelium can importantly modulate the response to serotonin. While in normal arteries, the cells inhibit the vasoconstrictor effects of the monoamine, the endothelium facilitates its contractions in atherosclerotic and hypertensive blood vessels.
血清素在心血管系统中有多种相反的作用。血管内皮作为血清素心血管效应的调节剂和介质起着重要作用。内皮细胞含有可使血清素失活的单胺氧化酶。此外，内皮细胞还是血管舒张物质的来源，如内皮衍生舒张因子，即内源性硝基血管舒张剂。动脉内皮持续生成一氧化氮以抑制血清素等血管收缩物质的作用。因此，在大多数血管标本中，去除内皮会增强血清素诱导的收缩。在某些血管中，如猪和犬的冠状动脉，血清素会刺激内皮衍生一氧化氮的释放。猪心肌内冠状动脉阻力动脉对血清素也会出现内皮依赖性舒张。与猪和犬的动脉不同，在人类冠状动脉和乳内动脉中尚未证实对血清素的内皮依赖性舒张。在再生内皮的猪冠状动脉和有动脉粥样硬化改变的猪冠状动脉中，内皮会促进对血清素的收缩，这表明会释放一种内皮衍生的收缩因子。由于吲哚美辛可阻止动脉粥样硬化猪冠状动脉中这种内皮依赖性的对血清素收缩的促进作用，因此可能涉及一种环氧化酶产物。同样，在自发性高血压大鼠的主动脉中，内皮会促进对血清素的收缩。因此，内皮可显著调节对血清素的反应。在正常动脉中，内皮细胞会抑制单胺的血管收缩作用，而在动脉粥样硬化和高血压血管中，内皮会促进其收缩。
