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 journalArticle

53 Citations (Scopus)

Abstract

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
JournalHypertension
Volume44
Issue number3
DOIs
StatePublished - Sep 1 2004

Fingerprint

Knockout Mice
Interleukin-6
Arterial Pressure
Motor Activity
Heart Rate
Blood Pressure
Phenylephrine
Renin
Angiotensin II
Area Under Curve
Norepinephrine
Perfusion
Cytokines
Equipment and Supplies

Keywords

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

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Hypertensive response to acute stress is attenuated in interleukin-6 knockout mice. / Lee, Dexter L.; Leite, Romulo; Fleming, Cassandra; Pollock, Jennifer S.; Webb, R. Clinton; Brands, Michael W.

In: Hypertension, Vol. 44, No. 3, 01.09.2004, p. 259-263.

Research output: Contribution to journalArticle

Lee, Dexter L. ; Leite, Romulo ; Fleming, Cassandra ; Pollock, Jennifer S. ; Webb, R. Clinton ; Brands, Michael W. / Hypertensive response to acute stress is attenuated in interleukin-6 knockout mice. In: Hypertension. 2004 ; Vol. 44, No. 3. pp. 259-263.
@article{a95166f218e24aa9bdb6e423006ee021,
title = "Hypertensive response to acute stress is attenuated in interleukin-6 knockout mice",
abstract = "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.",
keywords = "Blood pressure monitoring, Catecholamines, Cytokines, Mice, Renin, Sympathetic nervous system",
author = "Lee, {Dexter L.} and Romulo Leite and Cassandra Fleming and Pollock, {Jennifer S.} and Webb, {R. Clinton} and Brands, {Michael W.}",
year = "2004",
month = "9",
day = "1",
doi = "10.1161/01.HYP.0000139913.56461.fb",
language = "English (US)",
volume = "44",
pages = "259--263",
journal = "Hypertension",
issn = "0194-911X",
publisher = "Lippincott Williams and Wilkins",
number = "3",

}

TY - JOUR

T1 - Hypertensive response to acute stress is attenuated in interleukin-6 knockout mice

AU - Lee, Dexter L.

AU - Leite, Romulo

AU - Fleming, Cassandra

AU - Pollock, Jennifer S.

AU - Webb, R. Clinton

AU - Brands, Michael W.

PY - 2004/9/1

Y1 - 2004/9/1

N2 - 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.

AB - 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.

KW - Blood pressure monitoring

KW - Catecholamines

KW - Cytokines

KW - Mice

KW - Renin

KW - Sympathetic nervous system

UR - http://www.scopus.com/inward/record.url?scp=4444253600&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=4444253600&partnerID=8YFLogxK

U2 - 10.1161/01.HYP.0000139913.56461.fb

DO - 10.1161/01.HYP.0000139913.56461.fb

M3 - Article

C2 - 15289466

AN - SCOPUS:4444253600

VL - 44

SP - 259

EP - 263

JO - Hypertension

JF - Hypertension

SN - 0194-911X

IS - 3

ER -