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Glucocorticoid sensitivity of circulating monocytes in essential hypertension

Petra H Wirtz1, Roland von Känel, Karl Frey

  • 1Institute for Behavioral Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland.

American Journal of Hypertension
|June 5, 2004
PubMed

Insights

Essential hypertension is linked to higher monocyte inflammatory activity. This increased tumor necrosis factor-alpha release in hypertensive men is less responsive to glucocorticoid inhibition, potentially explaining heightened cardiovascular risk.

Area of Science:

  • Cardiovascular Science
  • Immunology
  • Hypertension Research

Background:

  • Essential hypertension is a major cardiovascular risk factor.
  • Monocyte cytokine production is implicated in atherosclerosis and acute coronary syndromes.
  • This study compares monocyte function in hypertensive versus normotensive individuals.

Purpose of the Study:

  • To investigate differences in stimulated monocyte cytokine release between hypertensive and normotensive subjects.
  • To assess the impact of glucocorticoid inhibition on monocyte cytokine release in both groups.
  • To explore potential mechanisms linking hypertension to increased atherosclerotic risk.

Main Methods:

  • 222 middle-aged male employees were studied, with 76 classified as hypertensive.
  • In vitro monocyte tumor necrosis factor-alpha release was measured after lipopolysaccharide stimulation.
  • Monocyte glucocorticoid sensitivity was determined by dexamethasone's inhibitory effect on TNF-alpha release.

Main Results:

  • Hypertensive subjects exhibited 11% higher lipopolysaccharide-stimulated TNF-alpha release compared to normotensive subjects.
  • Monocyte glucocorticoid sensitivity was 21% lower in hypertensive individuals, indicating reduced dexamethasone efficacy.
  • These findings remained significant after controlling for traditional cardiovascular risk factors.

Conclusions:

  • Circulating monocytes display heightened proinflammatory activity in hypertensive men.
  • This elevated inflammatory potential may contribute to the increased atherosclerotic risk associated with essential hypertension.
  • Reduced glucocorticoid sensitivity of monocytes represents a potential mechanism in hypertensive individuals.
Abstract

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