Free and Conjugated Dopamine in Pheochromocytoma, Primary Aldosteronism and Essential Hypertension
Free and Conjugated Dopamine in Pheochromocytoma, Primary Aldosteronism and Essential Hypertension
复制标题
嗜铬细胞瘤、原发性醛固酮增多症和原发性高血压中的游离和结合多巴胺
DOI：
10.1161/01.hyp.1.3.267
复制
发表时间：
1979
期刊：
影响因子：
8.3
通讯作者：
J. Genest
中科院分区：
文献类型：
--
作者：
O. Kuchel;N. Buu;P. Hamet;W. Nowaczynski;J. Genest
由于最近被认为是多巴胺(DA)的降压和利钠作用很难检测(血浆中通常检测不到游离DA)，我们用一种新开发的共联儿茶酚胺水解法测定了4例嗜铬细胞瘤、4例原发性醛固酮增多症和34例高血压患者选择性静脉插管或外周静脉采血后的游离和结合DA。16例正常人血浆DA含量为0.98±0.1 ng/ml(SE)，几乎100%为结合态，尿中DA排泄量为2±03 mg/min，其中79%为结合态。1例血压正常的发作期出现DA和肾上腺素的交替高分泌，其中一例与外周循环中大量释放高达5.5 ng/ml的游离DA有关。原发性醛固酮增多症患者血浆总DA升高(3.1±0.3 ng/ml)，可测游离DA升高(0.4±0.2 ng/ml)，尿中DA排泄量升高(53±1.5/g/min)。除1例双侧小结节增生症患者单侧肾上腺切除后持续高醛固酮增多症外，切除肾上腺后尿液中总或游离DA排泄量均降至正常水平。高血压病患者血浆结合多巴胺水平升高(1.98±03 ng/ml)，可能源于肾上腺流出游离和结合多巴胺，但游离和总尿多巴胺排泄量低于原发性醛固酮增多症患者(游离多巴胺0.19±0.04vs0.61±0.01，尿总多巴胺0.9±0.04vs5.3±1.5 mg/min)。结合多巴胺的测定可能反映了游离的快速结合的多巴胺的释放，补充了高血压患者的游离多巴胺测定。血浆结合多巴胺升高可能反映了嗜铬细胞瘤的内源性自主多巴胺释放，在原发性醛固酮增多症和高血压中具有适应性特征。尿中游离和结合的DA排泄似乎反映了多巴胺调节的钠，从而改变了醛固酮的钠保留作用。
SUMMARY Since the hypotensive and natrluretic role recently attributed to dopamine (DA) is difficult to test (free DA is usually undetectable in plasma) we measured free and conjugated DA by a newly developed method of hydrolysis of conjugated catecholamlnes in four pheochromocytoma, four primary aldosteronism and 34 essential hypertensive patients subjected to selective venous catheterization or peripheral venous sampling. The 16 control subjects had plasma DA of 0.98 ± 0.1 ng/ml (SE), almost 100% of which was conjugated, and a urinary excretion of 2 ± 03 fig/min of DA, 79% of which was conjugated.Patients with a predominantly norepinephrine-secreting pheochromocytoma had elevated conjugated plasma DA (6 ± 0.S vs 2.5 ± 03 ng/ml in non-pheochromocytoma hypertensive patients) even between paroxysms; in a rare case an alternating DA and epinephrine hypersecretion was detected during predominantly normotensive paroxysms, one of which was associated with the flooding of the peripheral circulation by up to 5.5 ng/ml of free DA.Patients with primary aldosteronism had elevated total plasma DA (3.1 ± 0 3 ng/ml), detectable free DA (0.4 ± 0.2 ng/ml) and an elevated total urinary DA excretion (53 ± 1.5 /ig/min). Following the removal of the aldosteronoma, urinary excretion of total or free DA decreased to normal levels, except in one patient with a bilateral micronodular hyperplasia in whom the hyperaldosteronism persisted after unilateral adrenalectomy. Patients with essential hypertension bad elevated conjugated plasma DA (1.98 ± 03 ng/ml), probably originating in an adrenal outflow of free and conjugated DA, but lower free and total urinary DA excretion than patients with primary aldosteronism (0.19 ± 0.04 vs 0.61 ± 0.01 for free DA and 0.9 ± 0.04 vs 5 3 ± 1.5 Mg/min for total urinary DA). Measurements of conjugated DA, which probably reflects the release of free rapidly conjugated DA, complement the free DA determination in hypertension. Elevated plasma conjugated DA probably mirrors the endogenous autonomous dopamine release in pheochromocytoma and has an adaptive character in primary aldosteronism and essential hypertension. Urinary free and conjugated DA excretion appears to reflect the dopamine modulated natriuresls, modifying the sodium-retaining action of aldosterone.