HORMONAL RESPONSES TO SALT IN NORMAL AND ESSENTIAL HYPERTENSION

在以往的研究中， 那些耐盐的人尿中多巴胺含量更高 比那些对盐敏感的更敏感。 耐盐患者还 抑制了他们的血浆去甲肾上腺素对高钠摄入的反应 而盐敏感患者则没有。 在以下国家进行的类似研究 正常受试者表明，当钠摄入量从9增加到 249 mEq/d，钠潴留仅略低于 耐盐性，但显著低于盐敏感性 患者 尿多巴胺与盐敏感组无差异 但明显低于耐盐患者。 血浆去甲肾上腺素也没有显着差异，在盐敏感 但显著高于耐盐患者， 抑制血浆去甲肾上腺素对高盐摄入的反应。 这些 结果表明，在高盐摄入期间， 抗盐性高血压患者的多巴胺能活性 超正常钠潴留;多巴胺能神经系统也可能 介导这些患者血浆去甲肾上腺素的超常下降， 患者 不抑制血浆的超常钠潴留 去甲肾上腺素可能部分介导血压升高， 在盐敏感性高血压患者摄入高钠时发生。

In previous studies of patients with normal renin essential hypertension those that were salt-resistant were shown to have higher urinary dopamine than those that were salt-sensitive. The salt-resistant patients also suppressed their plasma norepinephrine in response to a high-sodium intake whereas the salt-sensitive patients did not. Similar studies performed in normal subjects indicate that when sodium intake was increased from 9 to 249 mEq/d, sodium retention was only slightly less than that in the salt-resistant but significantly less than that in the salt-sensitive patients. Urinary dopamine did not differ from that in the salt-sensitive but was significantly lower than that in the salt-resistant patients. Plasma norepinephrine also did not differ from that in the salt-sensitive but was significantly higher than that in the salt-resistant patients who suppressed plasma norepinephrine in response to high-salt intake. These results suggest that during a high-salt intake supranormal renal dopaminergic activity in the salt-resistant hypertensives prevents supranormal sodium retention; the dopaminergic nervous system may also mediate the supranormal decrease in plasma norepinephrine in these patients. Supranormal sodium retention that does not suppress plasma norepinephrine may mediate, in part, the increase in blood pressure that occurs during a high-sodium intake in the salt-sensitive hypertensives.