How does salt raise blood pressure? A hypothesis.
How does salt raise blood pressure? A hypothesis.
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DOI：
10.1161/01.hyp.8.1.83
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发表时间：
1986
期刊：
影响因子：
8.3
通讯作者：
H. Gavras
中科院分区：
文献类型：
--
作者：
H. Gavras
文献中的现有数据表明，α 2-肾上腺素能受体激动剂具有显著的抑制作用，钠可减弱α 2-肾上腺素能受体对激动剂的亲和力，这些受体在中枢神经系统中的位置主要位于心血管调节部位，这些部位对交感血管收缩张力产生持续的紧张性抑制。本文提出钠通过降低中枢神经系统α 2-肾上腺素能受体对局部发生的激动剂神经递质的亲和力状态，导致交感神经抑制神经元的去抑制，并导致盐诱导高血压的肾上腺素能亢进状态，从而发挥其高血压作用的理论。
Existing data in the literature indicate that alpha 2-adrenergic receptor agonists have a profound hypotensive action, that sodium attenuates the affinity of alpha 2-adrenergic receptors for agonists, that the location of these receptors in the central nervous system is mainly at the sites of cardiovascular regulation, and that these sites exert a constant tonic inhibition of sympathetic vasoconstrictor tone. This article proposes the theory that sodium exerts its hypertensive action by decreasing the state of affinity of the alpha 2-adrenergic receptors of the central nervous system for locally occurring agonist neurotransmitters, which results in disinhibition of sympathoinhibitory neurons and leads to the hyperadrenergic state characteristic of salt-induced hypertension.