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Am J Physiol Heart Circ Physiol (July 1, 2004). doi:10.1152/ajpheart.00048.2004
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Submitted on January 21, 2004
Accepted on June 30, 2004

Endothelin-1 Mediates Cardiac Mast Cell Degranulation, Matrix Metalloproteinase Activation and Myocardial Remodeling in Rats

David B. Murray1*, Jason D. Gardner1, Gregory L. Brower1, and Joseph S. Janicki1

1 Department of Anatomy, Physiology, & Pharmacology, Auburn University, Auburn, Alabama, USA

* To whom correspondence should be addressed. E-mail: murradb{at}auburn.edu.

The objective of this study was to determine whether elevated circulating levels of endothelin-1 (ET-1) are capable of mediating left ventricular (LV) mast cell, degranulation and thereby induce matrix metalloproteinase (MMP) activation. Following administration of 20 pg/ml ET-1 to blood perfused isolated rat hearts, LV tissue was analyzed for signs of mast cell degranulation and MMP activation. Relative to control, ET-1 produced extensive mast cell degranulation as well as a significant increase in myocardial water content (78.8 ± 1.5 % vs. 74.2 ± 2.2 %, p<0.01), a marked 107% increase in MMP-2 activity (p<0.05), and a substantial decrease in collagen volume fraction (0.69 ± 0.09% vs. 99 ± 0.04%, p<0.001). Although the myocardial edema would be expected to increase ventricular stiffness compliance was not altered and moderate ventricular dilatation was observed (end diastolic volume at end diastolic pressure of 0 mmHg of 330.2 ± 22.1 µl vs. 298.9 ± 17.4 µl, ET-1 treated vs. control respectively, p=0.07). Additionally, pretreatment with the mast cell stabilizer, nedocromil prevented ET-1 induced changes in MMP-2 activity, myocardial water content, collagen volume fraction and end diastolic volume. These findings demonstrate that ET-1 is a potent cardiac mast cell secretogogue, and further indicate that ET-1 mediated mast cell degranulation is a potential mechanism responsible for myocardial remodeling.




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