Qing W, Dausse J P, Ben-Ishay D
Department of Pharmacology, INSERM U7/UA 318 CNRS, Hopital Necker, Paris, France.
Am J Hypertens. 1991 Mar;4(3 Pt 1):267-70. doi: 10.1093/ajh/4.3.267.
Sodium ions markedly decreased in vitro renal alpha 2-adrenoceptor affinity for epinephrine in Sabra hypertensive (SBH) but not in normotensive (SBN) rats. Under these conditions, affinity of alpha 1-adrenoceptor for epinephrine was unchanged in SBH and SBN rats. If these data could be confirmed in vivo, the sodium ion, by acting as an inhibitor, could modify the effect of agonists on renal alpha 2-adrenoceptors in SBH rats. Conversely, the absence of sodium regulation in SBN rats might represent a genetically mediated change responsible for the resistance to the development of salt-induced hypertension.
在体外实验中，钠离子显著降低了Sabra高血压（SBH）大鼠而非正常血压（SBN）大鼠肾脏α2 -肾上腺素能受体对肾上腺素的亲和力。在这些条件下，SBH和SBN大鼠中α1 -肾上腺素能受体对肾上腺素的亲和力未发生变化。如果这些数据能在体内得到证实，那么钠离子作为一种抑制剂，可能会改变激动剂对SBH大鼠肾脏α2 -肾上腺素能受体的作用。相反，SBN大鼠缺乏钠调节可能代表一种遗传介导的变化，这是其对盐诱导性高血压发展具有抗性的原因。
