Romero-Vecchione E, Vásquez J, Velasco M, Morales E, Davoli M A, Arocha I
Serv. de Cardiología, Hospital Vargas, Caracas.
Arch Inst Cardiol Mex. 1995 Nov-Dec;65(6):535-40.
Dopamine is synthetized and excreted by kidneys, this amine exerts its natriuretic and diuretic effects by inhibition of sodium reabsorption on kidney convoluted tubules. The objective of this study was to verify the changes of dopamine urinary excretion induced by nifedipine-LP treatment in hypertensive patients. Twenty four patients with essential hypertension (stages 1, 2) were included in this double-blind, placebo controlled study. Twelve patients received nifedipine (average daily dose, 21.5 mg/day) for 4 weeks, and 12 patients received placebo for the same time period. No significant changes were detected upon nifedipine treatment neither in plasma biochemical nor hematological parameters. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) was significantly reduced from pretreatment values 168.0 +/- 8.7 mmHg and 102.0 +/- 5.2 mmHg respectively, to end-treatment values 140.0 +/- 6.6 mmHg and 88.0 +/- 5.6 mmHg (p < 0.05). Placebo treatment did not modify SBP and DBP. Urinary dopamine excretion increased by 53% from 679.5 +/- 80.1 micrograms/24 h prior to treatment to 1040.0 +/- 110.1 micrograms/24 h after treatment (p < 0.009. 95% Confidence Interval of the Difference: -538.9 to -183.6). Urinary volume of nifedipine treated patients increased from 1613 +/- 85 mL/24 h to 1920 +/- 160 mL/24 h post-treatment (p < 0.05). No significant changes were observed in urinary noradrenaline and adrenaline excretion in nifedipine or placebo treated patients. Analysis of fluorescent light excitation and emission spectra (200 nm to 800 nm) of dopamine extracted from patient's urine submitted to nifedipine treatment did not reveal any interference when compared to chemically pure dopamine. If is concluded that nifedipine treatment of hypertensive patients increases kidney dopamine production which in turn can exert a natriuretic and diuretic effect besides its well known vasodilator properties.
多巴胺由肾脏合成和排泄，这种胺类物质通过抑制肾曲小管对钠的重吸收发挥其利钠和利尿作用。本研究的目的是验证硝苯地平-LP治疗对高血压患者尿多巴胺排泄的影响。24例原发性高血压（1、2期）患者纳入本双盲、安慰剂对照研究。12例患者接受硝苯地平（平均日剂量21.5mg/天）治疗4周，12例患者在同一时期接受安慰剂治疗。硝苯地平治疗后，血浆生化参数和血液学参数均未发现显著变化。收缩压（SBP）和舒张压（DBP）分别从治疗前的168.0±8.7mmHg和102.0±5.2mmHg显著降至治疗结束时的140.0±6.6mmHg和88.0±5.6mmHg（p<0.05）。安慰剂治疗未改变SBP和DBP。尿多巴胺排泄量从治疗前的679.5±80.1μg/24小时增加了53%，至治疗后的1040.0±110.1μg/24小时（p<0.009，差异的95%置信区间：-538.9至-183.6）。硝苯地平治疗患者的尿量从治疗前的1613±85mL/24小时增加至治疗后的1920±160mL/24小时（p<0.05）。硝苯地平或安慰剂治疗患者的尿去甲肾上腺素和肾上腺素排泄量未观察到显著变化。对接受硝苯地平治疗患者尿液中提取的多巴胺进行荧光激发和发射光谱分析（200nm至800nm），与化学纯多巴胺相比未发现任何干扰。得出结论：硝苯地平治疗高血压患者可增加肾脏多巴胺生成，这除了其众所周知的血管舒张特性外，还可发挥利钠和利尿作用。
