The effect of inhibition of intrarenal dopamine synthesis by carbidopa on the renal response to angiotensin II infusion was studied in six healthy salt-loaded volunteers. 2. Subjects received an infusion of angiotensin II at two doses (0.5 and 1.0 ng min-1 kg-1) on two occasions. Before one study they took a single dose of carbidopa (100 mg) by mouth. 3. The plasma concentrations of angiotensin II produced by the infusion were similar on both study days. Angiotensin II infusion reduced urinary dopamine excretion on the control day. Urinary dopamine excretion was undetectable at all times after carbidopa, but carbidopa did not change the basal excretion rate of sodium. Despite inhibition of renal dopamine synthesis, the reductions in both absolute and fractional sodium excretion during the angiotensin II infusion were not different from those seen in the control study. 4. The reductions in glomerular filtration rate and effective renal plasma flow which occurred during angiotensin II infusion were not modified by pretreatment with carbidopa. 5. The renal response to angiotensin II is not modulated either wholly or in part by endogenous intrarenal dopamine levels. The fall in urinary dopamine excretion which occurs during angiotensin II infusion is consistent with a modulatory role for tubular reabsorptive capacity in the regulation of proximal tubular dopamine synthesis.
摘要
在6名健康的盐负荷志愿者中,研究了卡比多巴抑制肾内多巴胺合成对肾脏对血管紧张素II输注反应的影响。2. 受试者在两个不同时间接受两种剂量(0.5和1.0 ng min-1 kg-1)的血管紧张素II输注。在一项研究前,他们口服单剂量卡比多巴(100 mg)。3. 输注产生的血管紧张素II血浆浓度在两个研究日相似。血管紧张素II输注在对照日降低了尿多巴胺排泄。卡比多巴给药后所有时间尿多巴胺排泄均无法检测到,但卡比多巴未改变钠的基础排泄率。尽管肾多巴胺合成受到抑制,但血管紧张素II输注期间绝对和分数钠排泄的降低与对照研究中观察到的情况没有差异。4. 血管紧张素II输注期间发生的肾小球滤过率和有效肾血浆流量的降低未因卡比多巴预处理而改变。5. 肾脏对血管紧张素II的反应并非全部或部分受内源性肾内多巴胺水平调节。血管紧张素II输注期间尿多巴胺排泄的下降与肾小管重吸收能力在近端肾小管多巴胺合成调节中的调节作用一致。