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Effects of corticotropin-releasing hormone (CRH) on monocyte function, mediated by CRH-receptor subtype R1 and R2: a

Ute Wilbert-Lampen1, Florian Straube, Anja Trapp

  • 1Medizinische Klinik und Poliklinik I, Klinikum Grosshadern, Ludwig-Maximillian-Universität, München, Germany. uwilbert@med.uni-muenchen.de

Journal of Cardiovascular Pharmacology
|January 21, 2006
PubMed

Insights

Stress hormone corticotropin-releasing hormone (CRH) increases monocyte adhesion and endothelin-1 release, contributing to endothelial dysfunction. CRH-receptor antagonists may prevent stress-related cardiovascular complications.

Area of Science:

  • Cardiovascular Science
  • Endocrinology
  • Immunology

Background:

  • Psychosocial factors are linked to coronary heart disease (CHD).
  • The mechanism of stress-induced endothelial dysfunction by corticotropin-releasing hormone (CRH) is unclear.
  • CRH is a key hormone in stress response.

Purpose of the Study:

  • Investigate extrahypothalamic CRH effects on monocyte/endothelium adhesion.
  • Elucidate CRH influence on monocytic endothelin-1 (ET-1) and nitric oxide (NO) release.
  • Identify CRH receptors involved in these processes.

Main Methods:

  • Cell adhesion assay.
  • Flow cytometry for MAC-1 expression.
  • ELISA/fluorometry for ET-1/NO release.
  • mRNA analysis for CRH receptors.
  • Use of CRH-receptor antagonist astressin.

Main Results:

  • CRH increased monocyte adhesion and MAC-1 expression in a time- and concentration-dependent manner.
  • CRH elevated monocytic ET-1 release and decreased NO release.
  • Endothelial ICAM-1 and VCAM-1 expression remained unchanged.
  • The CRH effects were blocked by astressin.

Conclusions:

  • Peripherally circulating CRH influences monocyte homeostatic properties.
  • CRH contributes to stress-related endothelial dysfunction.
  • CRH-receptor antagonists may offer a novel strategy to prevent cardiovascular complications.

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