Bernini G, Paci A, Sgrò M, Moretti A, Salvetti A
Istituto di Clinica Medica I, University of Pisa, Italy.
Am J Hypertens. 1998 Jan;11(1 Pt 1):1-7. doi: 10.1016/s0895-7061(97)00306-3.
The aim of our study was to evaluate whether adrenals are involved in the secretion of endogenous digitalis-like factor(s) with polarity similar to (or less than) that of ouabain (EDLF-1), and whether acute plasma volume expansion is a physiological releasing stimulus for this factor(s) in humans. For this purpose, we measured the concentration of this substance(s) by a human placenta radioreceptor assay (RRA) and by the Du-Pont-NEN ouabain-EIA (immunoreactive ouabain, I-Oua) in plasma C18-extracts of eight normotensives and six patients with bilateral adrenalectomy before and after acute salt loading (2 lt 0.9% NaCl/2 h). The study was repeated after 2 weeks of increased sodium intake (200 mEq/day). Under basal conditions, EDLF-1 by RRA and I-Oua were similar in adrenalectomized patients and in controls and were not significantly modified by saline infusion. After 15 days of high sodium intake, basal plasma EDLF-1 and I-Oua were not significantly different from prediet levels, both in adrenalectomized patients and controls and were likewise unaffected by saline loading. Saline infusion, by contrast, significantly (P < or = .05) suppressed hematocrit and PRA and increased ANP both in controls and in patients, either before or after prolonged high dietary sodium. Plasma aldosterone (ALD) was similarly reduced (P < .001) in controls and, as expected, was undetectable in adrenalectomized patients. Our data indicate that in adrenalectomized patients circulating levels of EDLF-1 and I-Oua are similar to those of controls and that, in both groups, acute saline loading before and after sodium repletion does not influence circulating levels of these compounds. These findings suggest that, at least in humans, adrenals are not the main source of endogenous digitalis-like factor(s) with polarity similar to (or less than) that of ouabain, and that plasma volume expansion may be not a sufficient stimulus for the release of this factor(s).
我们研究的目的是评估肾上腺是否参与分泌极性与哇巴因相似（或小于哇巴因）的内源性洋地黄样因子（EDLF-1），以及急性血容量扩张是否是该因子在人体中的生理释放刺激因素。为此，我们通过人胎盘放射受体分析法（RRA）以及杜邦-新英格兰核公司的哇巴因酶免疫分析法（免疫反应性哇巴因，I-Oua），对8名血压正常者和6名双侧肾上腺切除患者在急性盐负荷（2升0.9%氯化钠/2小时）前后血浆C18提取物中该物质的浓度进行了测量。在钠摄入量增加（200毫当量/天）2周后重复该研究。在基础条件下，肾上腺切除患者和对照组中通过RRA测得的EDLF-1和I-Oua相似，且盐水输注对其无显著影响。高钠摄入15天后，肾上腺切除患者和对照组的基础血浆EDLF-1和I-Oua与饮食前水平无显著差异，同样不受盐水负荷影响。相比之下，无论在长期高钠饮食之前还是之后，盐水输注均显著（P≤0.05）降低了对照组和患者的血细胞比容及肾素活性，并增加了心钠素。对照组血浆醛固酮（ALD）同样降低（P<0.001），且正如预期，肾上腺切除患者中未检测到醛固酮。我们的数据表明，肾上腺切除患者中EDLF-1和I-Oua的循环水平与对照组相似，且在两组中，钠补充前后的急性盐水负荷均不影响这些化合物的循环水平。这些发现表明，至少在人体中，肾上腺不是极性与哇巴因相似（或小于哇巴因）的内源性洋地黄样因子的主要来源，且血容量扩张可能不是该因子释放的充分刺激因素。
