Hypertensive response to acute stress is attenuated in interleukin-6 knockout mice

Dexter L. Lee, Romulo Leite, Cassandra Fleming, Jennifer S. Pollock, R. Clinton Webb, Michael W. Brands

Research output: Contribution to journalArticlepeer-review

62 Scopus citations


This study tested the hypothesis that the inflammatory cytokine, interleukin-6, contributes to the hypertensive response to acute psychosocial stress, caused by switching male mice to a cage previously occupied by a different male mouse. Male C57BL6 (WT) and interleukin-6 (IL-6) knockout (KO) mice were implanted with biotelemetry devices to monitor mean arterial pressure, heart rate, and motor activity in the unrestrained state. Baseline mean arterial pressure was 98±1 and 103±1 for WT and IL-6 KO mice. Cage switch increased mean arterial pressure by 42±2 mm Hg in WT mice, but this was blunted significantly in KO mice (31±3 mm Hg peak increase). Area under the curve for the first 90 minutes also was significantly less. Heart rate and motor activity increased similarly, and there also were no differences in the increases in plasma renin activity or plasma norepinephrine concentration between WT and KO mice. Thus, the acute hypertensive response to psychosocial stress depends significantly on IL-6, and the effect appears to be specific for blood pressure rather than to a global impairment in the response to stress. However, because perfusion of the isolated mesenteric bed with phenylephrine and chronic infusion of angiotensin II caused similar responses in WT and IL-6 KO mice, it is clear that future studies are needed to determine to what extent the acute blood pressure effect of IL-6 is stress-specific.

Original languageEnglish (US)
Pages (from-to)259-263
Number of pages5
Issue number3
StatePublished - Sep 2004


  • Blood pressure monitoring
  • Catecholamines
  • Cytokines
  • Mice
  • Renin
  • Sympathetic nervous system

ASJC Scopus subject areas

  • Internal Medicine


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