Renal excretion of prostaglandin metabolites, arginine vasopressin, and sodium during endotoxin and endogenous pyrogen induced fever in the goat

Abstract

Responses to intravenous injections of an endotoxin (E. coli-lipopolysaccharide, 1 microgram/kg b.wt.) and endogenous pyrogen were studied in euhydrated and hyperhydrated goats. The biphasic febrile response to the endotoxin was associated with a pronounced increase in the renal excretion of measured prostaglandin (PG) metabolites (11-ketotetranor PGF metabolites). This increase was time-correlated with the elevation of the rectal temperature, and (in hyperhydrated animals) with an inhibition of the water diuresis and an increase in renal excretion of arginine vasopressin (AVP). Other effects of the endotoxin were an immediate depression of renal Na and K excretion followed by the development of pronounced natriuresis, and a reduction of plasma Fe and Zn concentrations. The appearance of the febrile reactions (peripheral vasoconstriction and shivering) was accompanied by miosis. The maximum elevation of the rectal temperature was significantly greater during euhydration than during hyperhydration. Also endogenous pyrogen elicited miosis concomitant with febrile reactions, and an elevation of the renal excretion of PG metabolites which was closely correlated in time with the monophasic febrile response, and (during hyperhydration) with temporary inhibition of the water diuresis and an increase in the renal AVP excretion. However, the responses were much weaker than the corresponding endotoxin effects. No appreciable changes in renal excretion of Na and K were observed in response to the endogenous pyrogen. It is concluded that the observed effects on renal cation excretion were manifestations of direct endotoxin influences on kidney function.(ABSTRACT TRUNCATED AT 250 WORDS)

Transient type 1 pseudo-hypoaldosteronism: report on an eight-patient series and literature review

“…Bacterial endotoxin increases renal production of prostaglandins, thromboxane, leukotrienes, IL-1 and endothelin [53][54][55]. Endotoxins cause natriuresis, either by direct action [53] or mediated by IL-1 [56].…”

Role of Atrial Natriuretic Peptide in Interleukin 1.BETA.-Induced Natriuresis in Conscious Rats.

“…Beasley et al (1988) reported that IL-1/3 gave rise to natriuresis and diuresis, but not kaliuresis accompanied by increased urinary excretion of PGE2 in conscious rats without a change in renal hemodynamics. Jonasson et al (1984) showed that exogenous and endogenous pyrogens increased urinary excretion of Na and PG metabolites in goats. In these studies, however, the occurrence of increases in urine Na excretion was not in accord with the increased urinary excretion of PGE2 and PG metabolites.…”

“…However, the exact mechanisms whereby cytokines increase urinary Na excretion and urine flow remain to be unknown and are still controversial (Gombos et al 1967;Levenson et al 1982; Jonasson et al 1984;Caverzasio et al 1987; Beasley et al 1988;Kohan 1989). Namely, pyrogen and cytokines have been found to stimulate the production of renal prostaglandins (PGs) with resultant increases in renal blood flow and direct inhibition of tubular Na reabsorption, which leads to a natriuresis and diuresis (Jonasson et al 1984; Beasley et al 1988;Kohan 1989). On the other hand, ibuprofen, indomethacin and acetylsalicylic acid, cycloxygenase inhibitors, have been reported to fail to inhibit a cytokine-induced natriuresis (Gombos et al 1967;Caverzasio et al 1987; Beasley et al 1988).…”

“…It is well known that the formation of pyrogen and cytokines in response to infection and inflammation brings about a natriuresis and diuresis (Brandt et al 1956; Gombos et al 1967;Beisel 1977;Jonasson et al 1984). However, the exact mechanisms whereby cytokines increase urinary Na excretion and urine flow remain to be unknown and are still controversial (Gombos et al 1967;Levenson et al 1982; Jonasson et al 1984;Caverzasio et al 1987; Beasley et al 1988;Kohan 1989).…”

Fever and fever syndrome. Current problems.

“…These responses can be related to local inflammatory responses which are induced by mononuclear cell factor (MCF). The elevation of circulating PG's and enhanced renal excretion of PG metabolites, especially during the early phase of fever, might further bear some relationship with altered organ functions during fever, e.g., the sequence of antidiuresis and diuresis observed in goats during endotoxin fever [30] or the dissociation of renal blood flow and local sympathetic activity [41].…”