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人类乳腺动脉和软静脉的微量胺诱导血管收缩

Kenneth J Broadley¹, Dheeraj Mehta²

¹Division of Pharmacology, Cardiff School of Pharmacy and Pharmaceutical Sciences, Cardiff University, King Edward Vll Avenue, Cardiff, Wales CF10 3NB, UK.

Vascular pharmacology

|July 3, 2023

概括

β-乙烯胺 (PEA) 在人体动脉和静脉中引起显著的血管收缩,可能由微量胺相关受体 (TAARs) 而不是α1-上腺受体介导. 这挑战了PEA在人类血管系统上被归类为同情胺胺的分类.

科学领域:

药理学药理学是指药理学的学科.
心血管生理学心血管生理学

背景情况:

众所周知,像β-phenylethylamine (PEA) 这样的交感类胺可以收缩动物的血管.
作用机制被认为涉及微量胺相关受体 (TAARs),而不是α-上腺受体和动物中的诺亚上腺素释放.
这种机制尚未在人类血管中确立.

研究的目的:

调查PEA是否会导致人体动脉和静脉的血管收缩.
为了确定人体血管中PEA诱导的血管收缩是否由上腺受体介导.

主要方法:

在隔离的人体内部乳腺动脉和沙静脉环上进行了功能性研究.
异度收缩被测量为对PEA和α-腺受体agonistphenylephrine的累积度的反应.
评估了α1-上腺素受体对抗剂普拉佐辛的作用.

主要成果:

在人类的乳腺动脉和软静脉中,PEA诱导了与度相关的收缩.
与PEA诱导的收缩相比,PEA诱导的收缩发展速度较慢,并且与非尼莱弗林相比,收缩趋于平稳.
α1-上腺素受体对抗剂普拉佐辛没有阻止PEA诱导的收缩,这表明非α1-上腺素受体介导的机制.
烯诱导的收缩被普拉佐辛阻断.

结论:

β-乙烯胺 (PEA) 在人体阴静脉和乳腺动脉中引起大量血管收缩.
人体血管中对PEA的血管收缩反应可能是由TAARs介导的,而不是α1-上腺受体.
根据这些发现,PEA作为人类血管上的交感模拟氨酸的分类需要根据这些发现进行修订.

关键词:

人类的乳腺动脉.人类的沙芬静脉.微量氨基相关受体微量氨基相关受体微量氨基的微量氨基.这是一种β-phenylethylamine.

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Physical Properties of Amines

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