A_2A受体-EETs途径在盐敏感性高血压治疗中的作用

Effects of the adenosine 2A receptor-epoxyeicosatrienoic acids pathway in the treatment of salt-sensitive hypertension

激活大鼠腺苷2A受体(A2A R)可使表氧化酶活性增强,从而提高环氧二十碳三烯酸(EETs)的水平,因EETs有扩张肾血管、降血压等作用,故A2A R-EETs途径有抗升压作用。通过盐敏感性高血压遗传模型Dahl盐敏感性(Dahl SS)大鼠和Dahl盐抵抗性(Dahl SR)大鼠的相关实验得知,高盐喂养的Dahl SR大鼠,其腺苷水平及肾脏对腺苷的反应性均提高,使其表氧化酶活性和EETs的水平升高,因而引发更加明显的肾血管舒张反应,即Dahl SR大鼠可通过上调A2A REETs途径来调节盐负荷时的血压水平;而Dahl SS大鼠却无上述调节能力。因此在盐负荷时上调Dahl SS大鼠的A2A R-EETs途径,有利于治疗盐敏感性高血压。

Activation of rat adenosine 2A receptors （A2a R） increases epoxygenase activity and epoxyeicosatrienoic acids （EETs） levels. Since EETs have the abilities to dilate the renal vessels and prevent elevation of blood pressure, the adenosine 2A receptor-epoxyeicosatrienoic acids pathway （A2AR-EETs pathway） is an antipressor. The experiments of the Dahl salt-sensitive （SS） rats and the Dahl salt resistant （SR） rats show that in the Dahl SR rats fed a high salt （HS） diet, elevations of adenosine levels and the renal response to adenosine increase epoxygenase activity and EETs levels, resulting in a greater renal vasodilator. In other words, the Dahl SR rats are able to upregulate the A2AR-EETs pathway to regulate blood pressure during salt loading. However, the Dahl SS rats don＇t have the a- bove-mentioned capabilities. Thus upregulating the A2aR-EETs pathway in the inability of Dahl SS rats during salt loading may contribute to the treatment of salt-sensitive hypertension.