Atrial natriuretic peptide (ANP) responsiveness in patients with hypothyroidism.

Acta medica Hungarica Pub Date : 1994-01-01
I Barna, J Földes, M Tóth, B Büki, R E Lang, R De Châtel
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Abstract

Hypothyroidism is known to be associated with abnormalities of kidney function; recently, low atrial natriuretic peptide (ANP) plasma levels have been reported. Aim of the study was to asses ANP, sodium and water responsiveness to an acute saline load. Twelve patients with established primary hypothyroidism and 9 control subjects were studied. ANP was determined in plasma by RIA with extraction, prior to and after the infusion of saline, 500 ml/h for 4 hours. On a similar albeit liberal sodium diet hypothyroid patients excreted less sodium and water (74 +/- 33 (SD) mumol/min and 0.69 +/- 0.15 ml/min, respectively) than control subjects (110 +/- 52 mumol/min; P < 0.05 and 1.06 +/- 0.53 ml/min; P < 0.025, respectively). However, the infusion of saline resulted in a 3-fold increase of sodium output and more than 2-fold increase in urine flow. The exaggerated responsiveness in sodium excretion in patients with hypothyroidism was associated with significantly decreased pre-infusion ANP plasma levels (16.1 +/- 11.1 pg/ml vs. 44.4 +/- 14.4 pg/ml; P < 0.001) and also with sluggish response to the volume expansion (+24% vs. +48%). A significant correlation was found between serum T4 levels and plasma ANP concentrations in 8 patients (r = 0.689; P < 0.05). Although hypothyroid patients tend to retain sodium on a liberal salt diet, their kidney is capable of vigorously eliminating excess sodium when challenged with an acute saline load. This exaggerated responsiveness of sodium excretion can be demonstrated in spite of a sluggish response in ANP. Subnormal ANP levels in hypothyroidism are probably the result of thyroid deficiency.

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甲状腺功能减退患者心房钠素(ANP)的反应性。
众所周知,甲状腺功能减退症与肾功能异常有关;近年来,血浆中心房利钠肽(ANP)水平较低也有报道。本研究的目的是评估急性生理盐水负荷下ANP、钠和水的反应性。研究了12例原发性甲状腺功能减退症患者和9例对照组。在生理盐水500 ml/h输注4小时前后,用提取法测定血浆ANP。在类似的自由钠饮食中,甲状腺功能减退患者的钠和水排泄量(分别为74 +/- 33 (SD) mumol/min和0.69 +/- 0.15 ml/min)低于对照组(110 +/- 52 mumol/min;P < 0.05和1.06±0.53 ml/min;P < 0.025)。然而,输注生理盐水导致钠排泄量增加3倍,尿流量增加2倍以上。甲状腺功能减退患者钠排泄反应性增高与输注前ANP血浆水平显著降低相关(16.1 +/- 11.1 pg/ml vs. 44.4 +/- 14.4 pg/ml;P < 0.001),并且对体积扩张反应迟缓(+24% vs +48%)。8例患者血清T4水平与血浆ANP浓度有显著相关性(r = 0.689;P < 0.05)。虽然甲状腺功能减退患者倾向于在自由盐饮食中保留钠,但当急性盐负荷挑战时,他们的肾脏能够有力地消除多余的钠。尽管在ANP中反应迟缓,但可以证明这种钠排泄的夸大反应性。甲状腺功能减退症的ANP水平异常可能是甲状腺功能不足的结果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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Time-course changes in pancreatic laboratory and morphologic parameters in two different acute pancreatitis models in rats. Mitotic delay in peripheral blood lymphocytes and fibroblast cultures obtained from a child with Down's syndrome and from a healthy child. The reaction of adenohypophysis hormones in primary hyperparathyroidism and after surgical treatment. Atrial natriuretic peptide (ANP) responsiveness in patients with hypothyroidism. Hypothalamic dysfunction in Parkinson's disease patients.
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