Mark A L
Department of Internal Medicine, University of Iowa College of Medicine, Veterans Administration Medical Center, Iowa City.
Hypertension. 1991 Jan;17(1 Suppl):I86-90. doi: 10.1161/01.hyp.17.1_suppl.i86.
The Dahl strain provides a model for examining mechanisms involved in the genetic sensitivity or resistance to salt-induced hypertension. Dahl salt-sensitive rats develop hypertension when fed a high salt diet; Dahl salt-resistant rats remain normotensive. Based on early experiments, it was thought that hypertension in Dahl salt-sensitive rats epitomized the overriding importance of renal and humoral mechanisms in salt-induced hypertension, but studies in the past 15 years have demonstrated that alterations in sympathetic neural mechanisms also participate critically in the genetic predisposition to salt-induced hypertension in Dahl salt-sensitive rats. This article briefly reviews sympathetic neural mechanisms in Dahl rats, including evidence for a role of afferent baroreceptor as well as central neural and peripheral adrenergic mechanisms in salt-induced hypertension in Dahl salt-sensitive rats.
达尔品系为研究对盐诱导性高血压的遗传易感性或抗性所涉及的机制提供了一个模型。给达尔盐敏感大鼠喂食高盐饮食时会出现高血压;达尔盐抗性大鼠则保持血压正常。基于早期实验,人们认为达尔盐敏感大鼠的高血压体现了肾脏和体液机制在盐诱导性高血压中的首要重要性,但过去15年的研究表明,交感神经机制的改变在达尔盐敏感大鼠对盐诱导性高血压的遗传易感性中也起着关键作用。本文简要回顾了达尔大鼠中的交感神经机制,包括传入压力感受器以及中枢神经和外周肾上腺素能机制在达尔盐敏感大鼠盐诱导性高血压中作用的证据。