Hansell P, Källskog O, Wolgast M
Department of Physiology and Medical Biophysics, University of Uppsala, Sweden.
Kidney Blood Press Res. 1996;19(2):109-14. doi: 10.1159/000174052.
Dopamine (DA) is a natriuretic hormone synthesized in the kidneys by conversion of filtered 3,4-dihydroxyphenylalanine (L-Dopa), and is activated during hypervolaemia and increased dietary sodium intake. The natriuretic activity of endogenous DA is controversial, however, and the regulation of renal DA synthesis has yet to be explained. It has been suggest that the adrenals may be major suppliers of plasma L-Dopa on the basis of their catecholamine biosynthesis. A study was conducted in rats to elucidate the role of the adrenal glands as dynamic suppliers of L-Dopa to plasma, and thereby as sources of urinary DA. Adrenal venous and systemic arterial plasma concentrations and urinary excretion of L-Dopa, DA and sodium were measured before and during acute isotonic volume expansion (VE; 5% of body weight). One group of animals were acutely adrenalectomized (ADX group) to elucidate the ultimate importance of the adrenals in VE-induced renal sodium and DA excretion. In intact animals, the L-Dopa concentration was 62% higher in adrenal venous than in systemic arterial plasma under control conditions, and 42% higher during VE. The adrenaline concentration was 65 times higher in adrenal venous than in systemic arterial plasma before VE and 56 times higher during VE. The L-Dopa concentration in systemic arterial plasma and the urinary L-Dopa excretion were similar in intact and ADX animals. In intact animals, renal sodium and DA excretion during VE increased more than 13-fold and by 42%, respectively. The corresponding values in ADX animals did not differ from those in the intact animals (more than 14-fold and 36%, respectively). It is concluded that the adrenal glands are only minor suppliers of plasma L-Dopa and minor sources of urinary DA. The regulation of plasma L-Dopa remains to be explained.
多巴胺（DA）是一种利钠激素，由滤过的3,4-二羟基苯丙氨酸（L-多巴）在肾脏中转化合成，在血容量过多和饮食中钠摄入量增加时被激活。然而，内源性DA的利钠活性存在争议，并且肾脏DA合成的调节机制尚未得到解释。有人提出，基于肾上腺的儿茶酚胺生物合成，肾上腺可能是血浆L-多巴的主要供应者。本研究在大鼠中进行，以阐明肾上腺作为L-多巴向血浆动态供应者的作用，从而作为尿DA来源的作用。在急性等渗容量扩张（VE；体重的5%）之前和期间，测量肾上腺静脉和全身动脉血浆中L-多巴、DA和钠的浓度以及尿排泄量。一组动物进行急性肾上腺切除术（ADX组），以阐明肾上腺在VE诱导的肾钠和DA排泄中的最终重要性。在完整动物中，在对照条件下，肾上腺静脉中的L-多巴浓度比全身动脉血浆中的高62%，在VE期间高42%。在VE之前，肾上腺静脉中的肾上腺素浓度比全身动脉血浆中的高65倍，在VE期间高56倍。完整动物和ADX动物的全身动脉血浆中L-多巴浓度和尿L-多巴排泄量相似。在完整动物中，VE期间肾钠和DA排泄分别增加了13倍以上和42%。ADX动物的相应值与完整动物的相应值没有差异（分别超过14倍和36%）。结论是，肾上腺只是血浆L-多巴的次要供应者和尿DA的次要来源。血浆L-多巴的调节机制仍有待解释。
