Iimura O, Shimamoto K, Ura N
Second Department of Internal Medicine, Sapporo Medical College, Japan.
J Cardiovasc Pharmacol. 1990;16 Suppl 7:S56-8.
To investigate whether the suppression of the renal dopaminergic system in hypertension is primary or secondary, renal dopaminergic activity was compared between young healthy normotensive subjects without a family history of hypertension [FH(-)] and those with a family history of hypertension [FH(+)]. A significant decrease in urinary dopamine excretion was recognized, and the responses of urine volume, urinary sodium excretion, fractional excretion of sodium, and urinary kallikrein and kinin activity to infused dopamine were significantly augmented in FH(+) subjects. In addition, a normal level of L-dopa delivery into the kidney and at the renal proximal tubules and a significant reduction of the conversion from L-dopa to dopamine in the kidney were found in FH(+) subjects. These findings suggest that renal dopaminergic activity is already suppressed at the prehypertensive stage, and a reduction in the conversion from L-dopa to dopamine in the proximal tubules may contribute to the attenuation of renal dopaminergic activity in FH(+) subjects.
为研究高血压患者肾多巴胺能系统的抑制是原发性还是继发性，我们比较了无高血压家族史的年轻健康血压正常受试者[FH(-)]和有高血压家族史的受试者[FH(+)]的肾多巴胺能活性。结果发现，FH(+)受试者的尿多巴胺排泄显著减少，且尿量、尿钠排泄、钠分数排泄以及尿激肽释放酶和激肽活性对输注多巴胺的反应显著增强。此外，在FH(+)受试者中发现，进入肾脏和肾近端小管的左旋多巴水平正常，但肾脏中左旋多巴向多巴胺的转化显著减少。这些发现表明，在高血压前期肾多巴胺能活性就已受到抑制，近端小管中左旋多巴向多巴胺转化的减少可能导致FH(+)受试者肾多巴胺能活性减弱。
