Barendregt J N, van Nispen tot Pannerden L A, Chang P C
Department of Nephrology, University Hospital Leiden, The Netherlands.
J Hum Hypertens. 1994 Oct;8(10):747-54.
The involvement of the sympathetic nervous system and the renin-angiotensin-aldosterone system in renal dopamine (DA) synthesis and sodium excretion (UNaV) were studied in 11 healthy volunteers. On a low sodium diet (LoSo, 50 mmol Na+) saline infusions were given without pretreatment or after oral intake of 50 mg captopril or 300 micrograms clonidine. On a high sodium diet (HiSo, 250 mmol Na+) saline was infused without or after intake of 300 micrograms clonidine. UNaV, the excretion rates of the DA precursor 3,4-dihydroxyphenylalanine (DOPA; UDOPAV), DA (UDAV), and noradrenaline (NA; UNAV), hormonal parameters, blood pressure (BP), glomerular filtration parameters, blood pressure (BP), glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured. Saline infusion alone during LoSo increased natriuresis without changes in catechol excretion or suppression of plasma renin activity (PRA) or plasma aldosterone (PALD). Sympatho-inhibition by clonidine resulted in marked antinatriuresis, decrease in BP and decrease in UDOPAV and UDAV, whereas plasma DOPA, GFR, and ERPF remained unchanged. PRA and PALD rose as indication of activation of the RAA system, probably by the reduced renal perfusion pressure after clonidine. Captopril significantly stimulated the saline-induced natriuresis without affecting UDOPAV and UDAV. On HiSo, when sympathetic tone is relatively suppressed, saline infusion alone stimulated natriuresis but did not affect catechol excretion or PRA. In the first and second hour after saline infusion PALD was suppressed. Clonidine again reduced BP and natriuresis, while PRA, PALD, and UDOPAV and UDAV were unaffected. These results suggest that sympathetic nerve activity may stimulate the intrarenal DA production.(ABSTRACT TRUNCATED AT 250 WORDS)
在11名健康志愿者中研究了交感神经系统和肾素 - 血管紧张素 - 醛固酮系统对肾脏多巴胺（DA）合成及钠排泄（UNaV）的影响。在低钠饮食（LoSo，50 mmol Na +）情况下，在未进行预处理时或口服50 mg卡托普利或300 μg可乐定后给予生理盐水输注。在高钠饮食（HiSo，250 mmol Na +）情况下，在未摄入或摄入300 μg可乐定后输注生理盐水。测量了UNaV、DA前体3,4 - 二羟基苯丙氨酸（DOPA；UDOPAV）、DA（UDAV）和去甲肾上腺素（NA；UNAV）的排泄率、激素参数、血压（BP）、肾小球滤过参数、肾小球滤过率（GFR）和有效肾血浆流量（ERPF）。在LoSo期间单独输注生理盐水可增加尿钠排泄，而儿茶酚胺排泄无变化，血浆肾素活性（PRA）或血浆醛固酮（PALD）也未受抑制。可乐定引起的交感神经抑制导致明显的尿钠排泄减少、血压下降以及UDOPAV和UDAV降低，而血浆DOPA、GFR和ERPF保持不变。PRA和PALD升高表明RAA系统被激活，可能是由于可乐定后肾灌注压降低所致。卡托普利显著刺激了生理盐水诱导的尿钠排泄，但不影响UDOPAV和UDAV。在HiSo时，当交感神经张力相对受抑制时，单独输注生理盐水刺激尿钠排泄，但不影响儿茶酚胺排泄或PRA。在输注生理盐水后的第一和第二小时，PALD受到抑制。可乐定再次降低血压和尿钠排泄，而PRA、PALD、UDOPAV和UDAV未受影响。这些结果表明交感神经活动可能刺激肾内DA的产生。（摘要截取自250字）
