Thromb Haemost 2007; 98(05): 944-951
DOI: 10.1160/TH07-02-0128
Theme Issue Article
Schattauer GmbH

Adrenomedullin and endothelial barrier function

Bettina Temmesfeld-Wollbrück
1   Department of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité – Universitätsmedizin Berlin, Berlin, Germany
,
Andreas C. Hocke
1   Department of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité – Universitätsmedizin Berlin, Berlin, Germany
,
Norbert Suttorp
1   Department of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité – Universitätsmedizin Berlin, Berlin, Germany
,
Stefan Hippenstiel
1   Department of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité – Universitätsmedizin Berlin, Berlin, Germany
› Author Affiliations

Financial support:This work was supported by the Deutsche Forschungsgemeinschaft to S.H. (HI 789/6–1), and the Bundesministerium für Bildung und Forschung to S. H. and N. S. (BMBF-Competence Network CAPNETZ and PROGRESS), and the Charité –Universitätsmedizin Berlin to B. T.-W. (Rahel-Hirsch award).
Further Information

Publication History

Received 19 February 2007

Accepted after resubmission 12 July 2007

Publication Date:
30 November 2017 (online)

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Summary

Although loss of endothelial barrier function is a hallmark of every acute inflammation and contributes to fatal loss of organ function during severe infections, there is no sufficient therapy for stabilization of endothelial barrier function. Endogenous peptide adrenomedullin (AM) serum levels were shown to be increased during severe infection including sepsis and septic shock. In different in-vitro and in-vivo models AM acted as a potent therapeutic endothelial barrier function-stabilizing agent. Activation of specific receptors by AM results in elevation of second messenger cAMP. AM inhibits actin-myosin based endothelial cell contraction and junctional disassembly, thereby preventing paracellular permeability and oedema formation. The peptide furthermore possesses several protective cardiovascular qualities, including protection of the microcirculation during inflammation, and was proven as an efficient counter-regulatory molecule in various models of sepsis and septic shock. Overall, AM may be an attractive molecule to combat against cardiovascular malfunction during severe infection.