Janssen W M, de Zeeuw D, van der Hem G K, de Jong P E
Department of Medicine, University Hospital Groningen, The Netherlands.
J Hypertens. 1994 Apr;12(4):439-47.
To study the tubular site or sites of the natriuretic action of atrial natriuretic factor and the possible differences between healthy subjects and patients with essential hypertension.
Nine healthy volunteers and six patients with essential hypertension were studied on four test days under standard conditions, water loading and hydropenia with mannitol or saline loading. On each test day baseline, atrial natriuretic factor infusion (1 microgram/min) and recovery measurements were performed after equilibrium had been reached. The measurements included the atrial natriuretic factor (ANF) plasma levels, blood pressure, glomerular filtration rate (GFR), effective renal plasma flow, urinary osmolality and the (fractional) excretions of (free) water, sodium and potassium.
Fractional free-water excretion and free-water reabsorption (as a function of osmolar clearance) were calculated during water loading and hydropenia with mannitol or saline loading, respectively, using standard formulae. [125I]-iothalamate and [131I]-hippuran were infused continuously for the measurement of GFR and effective renal plasma flow, respectively.
The plasma ANF concentration rose five- to eightfold during the infusion of ANF, which induced an increase in urinary sodium excretion, a small increase in GFR and a decrease in the effective renal plasma flow. Moreover, ANF induced an increase in fractional free-water excretion and a decrease in fractional free-water reabsorption. These changes did not correlate with changes in GFR. The blood pressure and potassium excretion were not affected. The effects of ANF on the plasma ANF levels, natriuresis and renal haemodynamics did not differ between the normotensive and the essential hypertensives. However, the increase in fractional free-water excretion was significantly greater in the patients with essential hypertension and correlated significantly with blood pressure (r = 0.56, P < 0.05).
These results indicate that the infusion of ANF at a low dose induces a similar natriuretic response in normotensive subjects and in patients with essential hypertension. This natriuresis is probably the result of both a glomerular and a tubular effect of ANF. Proximal as well as distal tubular sites seem to be involved. In essential hypertension an enhanced proximal as well as an impaired distal tubular action of ANF can be hypothesized.
研究心房利钠因子利钠作用的肾小管部位，以及健康受试者与原发性高血压患者之间可能存在的差异。
在标准条件下、水负荷及用甘露醇或盐水负荷造成缺水的4个试验日，对9名健康志愿者和6名原发性高血压患者进行研究。在每个试验日，在达到平衡后进行基线、心房利钠因子输注（1微克/分钟）及恢复测量。测量项目包括心房利钠因子（ANF）血浆水平、血压、肾小球滤过率（GFR）、有效肾血浆流量、尿渗透压以及（游离）水、钠和钾的（分数）排泄。
分别在水负荷及用甘露醇或盐水负荷造成缺水期间，使用标准公式计算游离水分数排泄和游离水重吸收（作为渗透清除率的函数）。连续输注[125I] - 碘肽酸盐和[131I] - 马尿酸，分别用于测量GFR和有效肾血浆流量。
在输注ANF期间，血浆ANF浓度升高了5至8倍，这导致尿钠排泄增加、GFR略有增加以及有效肾血浆流量减少。此外，ANF导致游离水分数排泄增加，游离水分数重吸收减少。这些变化与GFR的变化无关。血压和钾排泄未受影响。ANF对血浆ANF水平、利钠作用和肾血流动力学的影响在血压正常者和原发性高血压患者之间没有差异。然而，原发性高血压患者的游离水分数排泄增加明显更大，并且与血压显著相关（r = 0.56，P < 0.05）。
这些结果表明，低剂量输注ANF在血压正常者和原发性高血压患者中诱导相似的利钠反应。这种利钠作用可能是ANF的肾小球和肾小管效应共同作用的结果。近端和远端肾小管部位似乎都参与其中。在原发性高血压中，可以推测ANF的近端作用增强以及远端肾小管作用受损。
