Caverzasio J, Rizzoli R, Dayer J M, Bonjour J P
Am J Physiol. 1987 May;252(5 Pt 2):F943-6. doi: 10.1152/ajprenal.1987.252.5.F943.
Administration of pyrogen or endotoxins such as Escherichia coli lipopolysaccharide can elicit a marked increase in urinary sodium excretion. This response occurs without any elevation in the filtered load of sodium and it does not appear to be prostaglandin mediated. The various effects produced by endotoxins appear to have interleukin-1 as a common mediator. In the present work, we have studied whether human recombinant interleukin-1 beta (hrIL-1) could affect the renal handling of sodium and thus, could be implicated in natriuretic response to pyrogens or endotoxins. We observed that hrIL-1 intravenously injected into conscious rats provokes a marked increase in sodium excretion. This natriuretic response was not associated with any increase in glomerular filtration rate (clearance of [3H]inulin), nor was it accompanied by significant changes in the urinary excretion of potassium, calcium, or inorganic phosphate. The only concomitant alteration was a decrease in urinary pH. Pretreatment with indomethacin abolished the effect of hrIL-1 on urinary pH but did not modify the natriuretic response. In conclusion, hrIL-1 elicits a selective decrease in tubular sodium reabsorption, which does not appear to involve a change in prostaglandin synthesis. This observation strongly suggests that interleukin-1 could be a key mediator in endotoxin-induced natriuresis.
给予热原或内毒素（如大肠杆菌脂多糖）可引起尿钠排泄显著增加。这种反应在钠滤过负荷未升高的情况下发生，且似乎不是由前列腺素介导的。内毒素产生的各种效应似乎都以白细胞介素-1作为共同介质。在本研究中，我们研究了重组人白细胞介素-1β（hrIL-1）是否会影响肾脏对钠的处理，从而是否与对热原或内毒素的利钠反应有关。我们观察到，静脉注射到清醒大鼠体内的hrIL-1会引起钠排泄显著增加。这种利钠反应与肾小球滤过率（[3H]菊粉清除率）的任何增加均无关，也未伴随钾、钙或无机磷酸盐尿排泄的显著变化。唯一伴随的改变是尿pH值降低。用吲哚美辛预处理可消除hrIL-1对尿pH值的影响，但不改变利钠反应。总之，hrIL-1引起肾小管钠重吸收选择性降低，这似乎不涉及前列腺素合成的变化。这一观察结果强烈表明，白细胞介素-1可能是内毒素诱导利钠作用的关键介质。
