Dobbins D E
Department of Physiology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814-4799, USA.
Am J Physiol. 1998 Feb;274(2):H650-4. doi: 10.1152/ajpheart.1998.274.2.H650.
Numerous endogenous vasoactive agents have been shown to cause lymphatic smooth muscle contraction. In this study, we assessed the ability of serotonin (5-HT) to alter lymphatic smooth muscle activity and elucidated the receptor mechanisms of 5-HT's actions. Both intralymphatic and intra-arterial administration of 5-HT significantly increased lymphatic smooth muscle activity in lymphatics perfused at constant flow, as indicated by an increase in lymphatic perfusion pressure. The 5-HT-induced increase in lymphatic perfusion pressure is attenuated but not blocked by the intra-arterial infusion of phentolamine, suggesting the involvement of alpha-adrenoreceptors and 5-HT receptors. Intralymphatic infusion of the 5-HT2-receptor-agonist alpha-methylserotonin significantly increased lymphatic perfusion pressure, either alone or when administered into an alpha-receptor blocked preparation, whereas the 5-HT1-receptor-agonist carboxyami-dotryptamine maleate did not effect the prenodal lymphatics. These data indicate that the lymphatic smooth muscle contraction produced by 5-HT is mediated both by lymphatic alpha-adrenoreceptors and 5-HT2 receptors.
众多内源性血管活性物质已被证明可引起淋巴管平滑肌收缩。在本研究中,我们评估了血清素(5-羟色胺,5-HT)改变淋巴管平滑肌活动的能力,并阐明了5-HT作用的受体机制。如淋巴管灌注压力升高所示,在恒流灌注的淋巴管中,经淋巴管内和动脉内给予5-HT均显著增加了淋巴管平滑肌活动。动脉内输注酚妥拉明可减弱但不能阻断5-HT诱导的淋巴管灌注压力升高,提示α-肾上腺素能受体和5-HT受体均参与其中。淋巴管内输注5-HT2受体激动剂α-甲基血清素,无论是单独使用还是在α受体阻断的制剂中使用,均显著增加了淋巴管灌注压力,而5-HT1受体激动剂马来酸羧胺色胺对节前淋巴管无影响。这些数据表明,5-HT引起的淋巴管平滑肌收缩是由淋巴管α-肾上腺素能受体和5-HT2受体共同介导的。