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Role of matrix metalloproteinases on vasoconstriction-induced acute-remodeling of resistance arterioles

Maureen P. Hynes*, Luis A. Martinez-Lemus*, Gerald A. Meininger*

*Department of Medical Physiology, College of Medicine, Texas A&M University System Health Science Center, College Station, Texas, USA


Objective—To evaluate the effect of matrix metalloproteinase inhibitor (MMPi) on the development of inward eutrophic remodeling during 4 hours of norepinephrine (NE)-induced vasoconstriction.

Design—Original study.

Animals—18 Male Sprague-Dawley rats.

Procedure—Rats were anesthetized, and the cremaster muscle was harvested.  The primary arteriole was isolated from the muscle, and subsequently constricted with NE, either alone or in the presence of an MMP-2 and -9 inhibitor, for 4 hours.  Two different concentrations of MMPi were used (6.0x10-7M and 1.2x10-6M).  The internal diameter of the vessel was measured with a video caliper throughout the experiment, and expressed as a percentage of the maximal diameter.

Results—In the experiment for MMPi (6.0x10-7M) and its control, arterioles showed significant change in their passive diameter after prolonged vasoconstriction.  There was no significant change in the vessels’ passive diameter for a greater concentration of MMPi or in the corresponding control (for both, n=4).  However, for these experiments, values showed a trend similar to MMPi (6.0x10-7M).

Conclusions and Clinical Relevance—Results suggest that MMP-2 and -9 play a role in neither the functional nor the inward eutrophic remodeling of resistance arterioles that occurs in response to prolonged vasoconstriction.   

Impact for Human Medicine—An understanding of inward eutrophic remodeling will help open new avenues for researchers pursuing understanding of diseases like hypertension, atherosclerosis, and diabetes mellitus.  These conclusions will lead our laboratory to look at the role of cellular receptors for the extracellular matrix to better understand their role in functional and inward remodeling.