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IL‐6 Knockout Significantly Attenuates AngII Hypertension, but not its Salt Sensitivity
Author(s) -
Lee Dexter L.,
Lane Katherine,
Labazi Hicham,
Fleming Cassandra,
Brands Michael W.
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.a310
Subject(s) - natriuresis , endocrinology , medicine , excretion , chemistry , mean arterial pressure , sodium , urinary system , blood pressure , heart rate , organic chemistry
Previous results from our laboratory indicate that Interleukin‐6 knockout (IL‐6 KO) mice have a significantly lower mean arterial pressure (MAP) than wild‐type (WT) mice during a high salt (HS) diet and AngII infusion, suggesting that IL‐6 plays an important role in mediating the rightward shift in the renal pressure‐natriuresis relationship caused by AngII. The goal of this study was to determine the salt‐sensitivity of that effect. Male WT and IL‐6 KO mice were implanted with biotelemetry devices and placed in metabolic cages to monitor MAP, water, food intake and urinary sodium excretion. Baseline MAP during a LS (.49% NaCl) diet was 112 ± 2.0 and 110 ± 2.6 mmHg, urinary sodium excretion was 0.35 ± 0.03 and 0.38 ± 0.05 mEq/2 days for WT and IL‐6 KO mice, respectively. Baseline MAP during a HS (4% NaCl) diet was 114 ± 2.36 and 108 ± 3.0 mmHg, urinary sodium excretion was 2.8 ± 1.0 and 3.96 ± 0.3 mEq/2 days for WT and IL‐6 KO mice, respectively. On day 5 of AngII (90 ng/min, s.c) and a LS diet, MAP reached 152 ± 7.0 and 134 ± 10 mmHg, urinary sodium excretion was not different during this period in WT and IL‐6 KO mice, averaging 0.58± 0.12 and 0.69 ± 0.08 mEq/2 days, respectively. On day 5 of AngII and a HS diet, MAP reached 164 ± 2.0 (WT) and 146 ± 8.0 mmHg (IL‐6 KO), urinary sodium excretion was 3.75 ± 0.8 and 4.39 ± 0.40 mEq/2 days for WT and IL‐6 KO mice, respectively. These data confirm our previous report that knockout of IL‐6 significantly attenuates AngII hypertension, and the parallel shift in the pressure‐natriuresis relationship suggests, in addition, that this effect of IL‐6 is not salt‐sensitive.(HL7416, HL56259, HL75625, T32‐HL66993)