Clark B A, Rosa R M, Epstein F H, Young J B, Landsberg L
Department of Medicine, Beth Israel Hospital, Harvard Medical School, Boston, MA 02215.
Hypertension. 1992 Jun;19(6 Pt 1):589-94. doi: 10.1161/01.hyp.19.6.589.
Biogenic amine metabolism may be altered in hypertension and thus contribute to its pathophysiology. This report describes an abnormality in dopamine excretion in hypertensive subjects in the postabsorptive state that persists despite an increase in dietary precursors for dopamine supplied by a protein meal. We studied seven normotensive and six nonmedicated hypertensive men after two different meals: 60 g protein and a noncaloric electrolyte-equivalent broth. Overall mean sodium excretion was 56% higher in the hypertensive group throughout both meal studies (p less than 0.01), implying higher chronic dietary sodium intake. Despite this, overall urinary excretion of dopamine tended to be lower in hypertensive than in normotensive subjects (p = 0.06). Hypertensive also differed from normotensive subjects in their response to protein feeding. In the normotensive subjects there was a 23% increase in urinary dopamine excretion (p less than 0.05), which was not seen after the noncaloric meal. In the hypertensive subjects, there was no change in urinary dopamine after the protein meal. In the normotensive subjects there was a 74% increase in sodium excretion (p less than 0.01) after the protein meal, but no significant change was seen in the hypertensive subjects. There were no differences in baseline renal plasma flow or glomerular filtration rate between the groups and no statistically significant differences between the groups in their renal hemodynamic responses to the meals. In summary, hypertensive subjects have less renal dopamine production for the amount of sodium ingested and a decreased renal dopamine production in response to a protein load as compared with normotensive subjects, consistent with a renal defect in conversion of DOPA to dopamine.
生物胺代谢在高血压中可能发生改变,从而促成其病理生理过程。本报告描述了处于吸收后状态的高血压患者多巴胺排泄异常,尽管蛋白质餐提供的多巴胺膳食前体增加,但这种异常仍然存在。我们研究了7名血压正常和6名未接受药物治疗的高血压男性在进食两种不同餐食后的情况:60克蛋白质餐和无热量的电解质等效肉汤。在两项餐食研究中,高血压组的总体平均钠排泄量始终高出56%(p<0.01),这意味着其慢性膳食钠摄入量更高。尽管如此,高血压患者的多巴胺总体尿排泄量往往低于血压正常者(p = 0.06)。高血压患者与血压正常者对蛋白质摄入的反应也有所不同。在血压正常者中,尿多巴胺排泄量增加了23%(p<0.05),而在无热量餐后未出现这种情况。在高血压患者中,蛋白质餐后尿多巴胺没有变化。在血压正常者中,蛋白质餐后钠排泄量增加了74%(p<0.01),但高血压患者未出现显著变化。两组之间的基线肾血浆流量或肾小球滤过率没有差异,并且两组对餐食的肾血流动力学反应也没有统计学上的显著差异。总之,与血压正常者相比,高血压患者摄入一定量钠时肾脏产生的多巴胺较少,并且对蛋白质负荷的肾脏多巴胺产生减少,这与多巴向多巴胺转化的肾脏缺陷一致。