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Interleukin‐6 does not contribute to the increase in renal endothelin production stimulated by high salt intake
Author(s) -
Boesen Erika I,
Pollock David M
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a765-a
Subject(s) - excretion , medicine , endocrinology , urine , chemistry , urinary system , urine flow rate , endothelin 1 , kidney , receptor
High salt intake stimulates production of certain inflammatory cytokines and enhances renal endothelin‐1 (ET‐1) production, as indicated by increased urinary ET‐1 excretion. Whether cytokines participate in the signaling cascade to increase ET‐1 production during high salt intake is unknown. As interleukin‐6 (IL‐6) stimulates ET‐1 production by cultured cells, we hypothesized that the increase in urinary ET‐1 excretion in response to high salt intake would be attenuated in IL‐6 −/− mice. After a 24‐hour baseline urine collection (normal 0.8% NaCl chow), wild type (WT) and IL‐6 −/− mice received either normal NaCl (NS) or 4% NaCl (HS) chow for 2 weeks. Urine was collected for 24 hours at the end of each week. Baseline urinary ET‐1 excretion rates, urine flows and Na + excretion rates were not significantly different between the four groups. Urine ET‐1 excretion rate was significantly increased (P < 0.01) in mice that received 4% NaCl chow for 2 weeks compared to mice on normal NaCl chow, but this effect did not differ significantly between WT and IL‐6 −/− mice (% change vs baseline: 40 ± 12% WT HS, 49 ± 17% IL‐6 −/− HS, 7 ± 11% WT NS, −6 ± 23% IL‐6 −/− NS). Urine flow and Na + excretion rate were also significantly increased (P < 0.001 and P = 0.0001 respectively) in mice receiving 4% NaCl chow compared to mice receiving normal NaCl chow, but these effects were similar in both genotypes. Thus IL‐6 does not participate in the increase in renal ET‐1 production stimulated by high salt intake.