Interleukin-1 decreases renal sodium reabsorption: possible mechanism of endotoxin-induced natriuresis

Journal Article · Fri May 01 00:00:00 EDT 1987 · Am. J. Physiol.; (United States)

OSTI ID:6864375

Caverzasio, J; Rizzoli, R; Dayer, J M; Bonjour, J P

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, the authors 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. They 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 (/sup 3/H)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.

• Research Organization: Univ. of Geneva (Switzerland)
• OSTI ID: 6864375
• Journal Information: Am. J. Physiol.; (United States), Vol. 252:5
• Country of Publication: United States
• Language: English

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550201* - Biochemistry- Tracer Techniques