Suzuki H, Kasai K, Naitoh T, Nakamura T, Shina H, Ieiri T, Takemura Y, Shimoda S
Nihon Naibunpi Gakkai Zasshi. 1980 Jul 20;56(7):973-82. doi: 10.1507/endocrine1927.56.7_973.
To evaluate the dopaminergic control of aldosterone secretion, the following experiments were performed on 10 normal subjects (3 men and 7 women, aged 21 approximately 69 yrs.), 16 diabetics (8 men and 8 women, aged 20 approximately 74 yrs.) and 7 patients with untreated hyperthyroidism (2 men and 5 women aged 16 approximately 58 yrs.). Blood samples were withdrawn from an intravenous cannula indwelled in an antecubital vein at 0, 15, 30, 45, 60, 90 and 120 min after intravenous injection of 10mg metoclopramide with a volus. Plasma aldosterone levels and plasma renin activities (PRA) were measured by radioimmunoassay. In normal subjects, plasma aldosterone levels were significantly increased from basal levels of 111.8 +/- 1.3 Opg/ml (Mean +/- S.E.) to 183.4 +/- 23.3pg/ml 15 min after an intravenous injection of metoclopramide and were sustained for about 90 min. This increase induced by metoclopramide was, however, abolished by pretreatment with 2.5mg of bromocriptine. It is suggested that metoclopramide and bromocriptine are in a competitive relationship at the level of dopaminergic receptor. In diabetics, the mean plasma level of aldosterone was as low as 66.3 +/- 8.7pg/ml, which was significantly lower than that in normal subjects (p less than 0.01), and aldosterone response to metoclopramide was significantly diminished. Although this tendency was more apparent in diabetics with such complications as neuropathy or retinopathy, aldosterone response to metoclopramide implied that aldosterone secretion was under dopaminergic inhibition in this hypoaldosteronemic state. While aldosterone responded well to metoclopramide, PRA was not significantly altered in this treatment in normal subjects and diabetics. In patients with untreated hyperthyroidism, aldosterone response was similar to that in normal subjects.
为评估多巴胺能对醛固酮分泌的控制，对10名正常受试者（3名男性和7名女性，年龄约21至69岁）、16名糖尿病患者（8名男性和8名女性，年龄约20至74岁）以及7名未经治疗的甲状腺功能亢进患者（2名男性和5名女性，年龄约16至58岁）进行了以下实验。在以10毫克甲氧氯普胺静脉推注后0、15、30、45、60、90和120分钟，从前臂肘前静脉留置的静脉套管中采集血样。采用放射免疫分析法测定血浆醛固酮水平和血浆肾素活性（PRA）。在正常受试者中，静脉注射甲氧氯普胺15分钟后，血浆醛固酮水平从基础水平的111.8±1.3皮克/毫升（平均值±标准误）显著升高至183.4±23.3皮克/毫升，并持续约90分钟。然而，甲氧氯普胺引起的这种升高被2.5毫克溴隐亭预处理所消除。这表明甲氧氯普胺和溴隐亭在多巴胺能受体水平上存在竞争关系。在糖尿病患者中，醛固酮的平均血浆水平低至66.3±8.7皮克/毫升，显著低于正常受试者（p<0.01），且醛固酮对甲氧氯普胺的反应明显减弱。尽管这种趋势在伴有神经病变或视网膜病变等并发症的糖尿病患者中更为明显，但醛固酮对甲氧氯普胺的反应表明在这种醛固酮减少状态下醛固酮分泌受多巴胺能抑制。在正常受试者和糖尿病患者中，虽然醛固酮对甲氧氯普胺反应良好，但该治疗对PRA无显著改变。在未经治疗的甲状腺功能亢进患者中，醛固酮反应与正常受试者相似。
