DOPA METABOLISM IN SALT-RESISTANT AND SALT-SENSITIVE HYPERTENSION

在之前对正常受试者的一项研究中，钠摄入量的增加 从每天9mEq增加到249mEq/天与 尿DOPA与血浆DOPA无明显变化。这些观察结果 提示钠给药增加了多巴酚丁胺的释放 到了肾脏。由于DOPA的排泄，先兆 多巴胺，与多巴胺的排泄平行，增加 多巴酚A的转运和肾脏对其摄取的增加 是导致多巴胺排泄增加的原因 伴随着钠摄入量的增加。由于多巴胺 耐盐(SR)和盐胁迫的排泄都是异常的。 敏感型(SS)高血压，异常的可能性 对多巴代谢相关因素进行了研究。关于钠的摄入量 在每天9mEq的情况下，SR和SS的DOPA排泄量是正常的两倍 SR患者多巴胺排泄量高于正常(P<0.01)。 当钠摄入量增加时，SR和SR的DOPA排泄量增加 SS分别减少47%和96%(而正常受试者为66%) 但尿多巴胺仅分别增加了18%和15%， (在正常受试者中这一比例为49%)。血浆DOPA正常，确实如此 不是零钱。结果表明，DOPA的形成是 SR和SS高血压患者增加，这可以解释 SR中多巴胺的异常形成。结果还表明， 肾脏摄取多巴或将其转化为多巴胺 在SS中受损。

In a previous study in normal subjects an increase in sodium intake from 9 mEq/day to 249 mEq/day was associated with an increase in urinary DOPA without a change in plasma DOPA. These observations suggested that sodium administration increased the delivery of DOPA to the kidney. Since the excretion of DOPA, the precursor of dopamine, paralleled the excretion of dopamine, the increased delivery of DOPA and its increased uptake by the kidney presumably was responsible for the increase in dopamine excretion that accompanied the increase in sodium intake. Since dopamine excretion is abnormal in both salt-resistant (SR) and salt- sensitive (SS) hypertension, the possibility that abnormalities in DOPA metabolism were responsible was studied. On a sodium intake of 9 mEq/day DOPA excretion was twice normal in both SR and SS and dopamine excretion in SR was higher (P less than 0.01) than normal. When sodium intake was increased DOPA excretion increased in SR and SS by 47% and 96%, respectively, (versus 66% in normal subjects) but urinary dopamine increased by only 18% and 15%, respectively, (versus 49% in normal subjects). Plasma DOPA was normal and did not change. The results indicate that the formation of DOPA is increased in SR and SS hypertensives and this could explain the supernormal formation of dopamine in SR. The results also indicate that the uptake of DOPA by the kidney or its conversion to dopamine is impaired in SS.