褪黑素
肌钙蛋白
血管平滑肌
内分泌学
内科学
收缩(语法)
收缩性
血管收缩
生物
肌肉收缩
化学
医学
血清反应因子
转录因子
生物化学
基因
平滑肌
作者
Gui-qiong Zheng,Wenjuan Tong,Bi-chen Yuan,Shi-yu Luo,Yaling Zhang,Shuhan Sun
出处
期刊:Journal of Cardiovascular Pharmacology
[Ovid Technologies (Wolters Kluwer)]
日期:2022-07-01
卷期号:Publish Ahead of Print
被引量:1
标识
DOI:10.1097/fjc.0000000000001322
摘要
Inositol 1, 4, 5-trisphosphate (IP3) signaling-mediated calcium release drives the contraction of vascular smooth muscles and hence regulates blood vessel volume and blood pressure. Melatonin supplementation has been suggested to be beneficial for hypertension. To determine whether the blood pressure–lowering effect of melatonin was accounted for by IP3 signaling, we evaluated the vasoconstriction response and IP3 signaling in isolated mouse thoracic aortic rings during melatonin incubation. C57BL/6 mice were given intraperitoneal injections daily with melatonin, and the systolic blood pressure and contractility of aortic rings from melatonin-treated mice were decreased, and the contraction suppression effect of melatonin was attributed to the impaired expression of contractile proteins in vascular smooth muscle cells rather than IP3 signaling. Our results further showed that melatonin increased the expression of γ-secretase, which could cleave and release the notch intracellular domain, and the notch intracellular domain prevented the transcription of contractile genes by interfering with the interaction between serum response factor and myocardin, the master regulator of contractile protein. In this article, we report a novel mechanism by which melatonin regulates smooth muscle contractility that does not depend on IP3 signaling.
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