Preserved cardiovascular homeostasis despite blunted acetylcholine‐induced dilation in mice with endothelial muscarinic M3 receptor deletion

Preserved cardiovascular homeostasis despite blunted acetylcholine‐induced dilation in mice with endothelial muscarinic M3 receptor deletion
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DOI:
10.1111/apha.13262
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发表时间:
2019-02
期刊:
影响因子:
6.3
通讯作者:
A. Rhoden;Jakob Speiser;B. Geertz;June Uebeler;K. Schmidt;C. de Wit;T. Eschenhagen
A. Rhoden;Jakob Speiser;B. Geertz;June Uebeler;K. Schmidt;C. de Wit;T. Eschenhagen
中科院分区:
医学1区
文献类型:
--
作者:
A. Rhoden;Jakob Speiser;B. Geertz;June Uebeler;K. Schmidt;C. de Wit;T. Eschenhagen

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M胆碱型乙酰胆碱受体(AChMR1-5)是副交感神经纤维释放神经递质乙酰胆碱(ACh)时细胞反应的基础。ACh是刺激内皮依赖性血管扩张的典型激动剂,但大多数血管缺乏副交感神经支配,这对内皮AChMR在体内的生理功能提出了疑问。AChM3R的全局缺失显示了在ACh诱导的体外血管扩张和食物摄取中的作用,但总体心血管稳态尚未得到彻底的检验。
Muscarinic acetylcholine receptors (AChMR1‐5) are fundamental for cellular responses upon release of the neurotransmitter acetylcholine (ACh) from parasympathetic nerve fibers. ACh is the prototypical agonist stimulating endothelium‐dependent dilation, but most blood vessels lack parasympathetic innervation, raising the question as to the physiologic function of endothelial AChMR in vivo. Global deletion of AChM3R revealed a role in ACh‐induced vasodilation in vitro and food uptake, but overall cardiovascular homeostasis has not been examined thoroughly.