Kotchen T A, Luke R G, Ott C E, Galla J H, Whitescarver S
Ann Intern Med. 1983 May;98(5 Pt 2):817-22. doi: 10.7326/0003-4819-98-5-817.
Both the inhibition of renin release by sodium chloride and salt-sensitive hypertension have been attributed to sodium. We evaluated the contribution of chloride to these responses to sodium chloride. In the Sprague-Dawley rat, acute and chronic administration of sodium salts other than sodium chloride failed to suppress plasma renin activity, whereas renin was inhibited by both sodium chloride and by selective chloride (without sodium) loading. Plasma renin activity was stimulated by selective chloride depletion. Similarly, in humans, plasma renin activity was suppressed by sodium chloride but not by sodium bicarbonate infusion. In a preliminary study in the Dahl salt-sensitive rat, in contrast to sodium chloride loading, sodium bicarbonate loading failed to produce hypertension. Thus, both the renin and possibly the blood pressure responses to sodium chloride are dependent on chloride.
氯化钠对肾素释放的抑制作用以及盐敏感性高血压都被归因于钠。我们评估了氯离子对这些氯化钠反应的作用。在斯普拉格 - 道利大鼠中，急性和慢性给予除氯化钠以外的钠盐未能抑制血浆肾素活性，而肾素受到氯化钠和选择性氯离子（无钠）负荷的抑制。选择性氯离子耗竭刺激血浆肾素活性。同样，在人类中，血浆肾素活性受到氯化钠抑制，但不受碳酸氢钠输注抑制。在对 Dahl 盐敏感性大鼠的初步研究中，与氯化钠负荷相反，碳酸氢钠负荷未能产生高血压。因此，对氯化钠的肾素反应以及可能的血压反应都依赖于氯离子。
