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Role of TNF‐α in the dependency of Angiotensin II hypertension on IL‐6
Author(s) -
Sturgis LaShon C,
Brands Michael W
Publication year - 2007
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.21.5.a590-a
Subject(s) - angiotensin ii , endocrinology , medicine , renin–angiotensin system , proinflammatory cytokine , tumor necrosis factor alpha , blood pressure , cytokine , isoflurane , secretion , chemistry , inflammation , anesthesia
Our laboratory has reported that chronic Angiotensin II (Ang II) infusion increases plasma concentration of IL‐6, and that preventing the increase in IL‐6, by using IL‐6 KO mice, attenuates Ang II hypertension. The mechanism by which Ang II increases IL‐6 has yet to be determined. However, the proinflammatory cytokine TNF‐alpha is an important stimulus for IL‐6 secretion. Therefore, this study aimed to determine the role of TNF‐alpha in the dependency of Ang II hypertension on IL‐6. Mice were divided randomly into 4 groups: WT, TNF‐alpha KO, WT + ANG, and TNF‐alpha KO + ANG, and were implanted with blood pressure biotelemetry devices and allowed to recover for 5–7 days. After the baseline period (4 days) the animals were placed on a 4% NaCl diet for a 4‐day high‐salt control period. The AngII animals then had Ang II (90 ng/min) 14‐day minipumps implanted subcutaneously under brief isoflurane anesthesia. High salt diet alone did not change MAP in either group. Ang II increased mean arterial pressure similarly by ~30 mmHg over the 14‐day infusion period in both the WT and KO groups. AngII infusion also increased plasma IL‐6 in the TNF‐KO mice from < 5 to 27+/− 8 pg/ml, thus suggesting that TNF was not required for the effect of AngII to stimulate IL‐6 secretion. These results suggest that neither the IL‐6 response nor the hypertensive response to chronic AngII‐salt is dependent on TNF‐alpha.