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Cardiovascular Research Advance Access originally published online on October 7, 2009
Cardiovascular Research 2009 84(3):339-340; doi:10.1093/cvr/cvp331
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Vasoconstriction: tightening the noose through MMPs

Jeffery S. Isenberg1,2,* and Sruti Shiva2,3,*

1 Division of Pulmonary Allergy and Critical Care, Department of Medicine, University of Pittsburgh, Pittsburgh, PA 15260, USA
2 Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA 15260, USA
3 Department of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, PA 15260, USA

* Corresponding authors: 10048 Biomedical Science Tower 3, 3501 Fifth Avenue, Pittsburgh, PA 15261, USA. Tel: +1 412 383 5424; fax: +1 412-383-9009 (J.S.I). 10041 Biomedical Science Tower 3, 3501 Fifth Avenue, Pittsburgh, PA 15261, USA. Tel: +1 412 383 5854; fax: +1 412-383-5888 (S.S.) E-mail address: jsi5@pitt.edu (J.S.I); sss43@pitt.edu (S.S.).

This editorial refers to ‘Maintenance of adrenergic vascular tone by MMP transactivation of the EGFR requires PI3K and mitochondrial ATP synthesis’ by P.R. Nagareddy et al., pp. 368–377, this issue.

The first 10% of the full text of this article appears below.

Arterial tone is dependent on a balance between agents that lead to relaxation of arterial vascular smooth muscle cells (VSMCs) and agents that cause contraction of the same. The process of contraction at a mechanical level requires interaction of structural proteins including myosin light chain 2 (MLC2) and actin. The interaction of these leads to force transduction and cell shortening, ultimately causing vessel diameter narrowing and increased resistance to blood flow. Physiological vasoconstrictors, such as norepinephrine, work through binding cell receptors on VSMCs and activating . . . [Full Text of this Article]


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