胆淤积大鼠口服钠负荷后尿钠减少:室容积和ANP的作用。

J. Casar, A. Valdivieso, J. A. Bravo, C. Chacón, M. Boric
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引用次数: 1

摘要

本研究的目的是评估心房利钠肽(ANP)-cGMP系统在急性口服钠负荷下胆汁淤积大鼠的电解质和体积处理中的作用。结扎和切开胆总管诱导胆汁淤积(n = 51)。对照组56只。术后3周,测定24小时尿量、钠、钾、cGMP、肌酐排泄量。3 d后,灌胃10 mmol/kg NaCl (1 M),测定尿排泄量6 h。在平行组大鼠中,在基础条件下或口服钠超载后1小时,测定血浆体积、电解质和ANP浓度、细胞外液体积(ECFV)和肾髓ANP诱导的cGMP产生。与对照组相比,胆汁淤积大鼠ECFV更大,血浆ANP更高(67.2 +/- 5.2 vs 39.7 +/- 3.5 pg/ml),但红细胞压积和血容量更低,且低钠血症。胆汁淤积大鼠的钠、钾排泄量和尿cGMP均高于对照组。NaCl超载后,胆汁淤积大鼠钠排泄量减少,但尿cGMP不变。钠超载1小时后,两组均出现高钠血症,但对照组大鼠ECFV和ANP升高(50.7 +/- 4.1 pg/ml),而胆固醇淤积大鼠ECFV不变,血浆容量和ANP降低(37.5 +/- 5.8 pg/ml)。anp诱导的肾髓质cGMP生成在胆固醇抑制大鼠和对照非负荷大鼠中相似(14.2 +/- 5.2 vs 13.4 +/- 2.6 fmol/min/mg)。负荷1小时后,两组的髓质cGMP产量均显著升高,两组间无差异(20.6 +/- 3.1 vs 22.7 +/- 1)。7 fmol /分钟/毫克)。我们的结论是,由于体液分布的差异,胆汁淤积大鼠急性口服钠负荷的钝化排泄与血浆ANP降低有关,而不能用肾脏对ANP的难耐性来解释。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Reduced natriuresis after oral sodium load in cholestatic rats: role of compartment volumes and ANP.
The purpose of this study was to assess the participation of the atrial natriuretic peptide (ANP)-cGMP system in electrolyte and volume handling of cholestatic rats submitted to an acute oral sodium load. Cholestasis was induced by ligation and section of the common bile duct (n = 51). Control rats were sham operated (n = 56). Three weeks after surgery, 24-hr urinary volume, sodium, potassium, cGMP and creatinine excretion were measured. Three days later, animals received 10 mmol/kg NaCl (1 M) by gavage, and urinary excretion was measured for 6 hr. In parallel groups of rats, plasma volume, electrolytes and ANP concentration, extracellular fluid volume (ECFV), and renal medullary ANP-induced cGMP production were determined in basal conditions or 1 hr after oral sodium overload. As compared with controls, cholestatic rats had a larger ECFV and higher plasma ANP (67.2 +/- 5.2 vs 39.7 +/- 3.5 pg/ml), but lower hematocrit and blood volume, and were hyponatremic. Cholestatic rats showed higher basal excretion of sodium, potassium, and volume than controls, but equal urinary cGMP. After the NaCl overload, cholestatic rats showed a reduced sodium excretion but equal urinary cGMP. One hr after sodium overload, both groups showed hypernatremia, but whereas in control rats ECFV and ANP increased (50.7 +/- 4.1 pg/ml), in cholestatic rats ECFV was unchanged, and plasma volume and ANP were reduced (37.5 +/- 5.8 pg/ml). ANP-induced cGMP production in renal medulla was similar in cholestatic and control nonloaded rats (14.2 +/- 5.2 vs 13.4 +/- 2.6 fmol/min/mg). One hr after the load, medullary cGMP production rose significantly in both groups, without difference between them (20.6 +/- 3.1 vs 22.7 +/- 1. 7 fmol/min/mg). We conclude that the blunted excretion of an acute oral sodium load in cholestatic rats is associated with lower plasma ANP due to differences in body fluid distribution and cannot be explained by renal refractoriness to ANP.
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