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Differential effects of collagenase and elastase on arteriolar vasomotor responses
Author(s) -
Clifford Philip S.,
Ella Srikanth R.,
Yang Yan,
Davis Michael J.,
Meininger Gerald A.,
Hill Michael A.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.951.5
Subject(s) - elastin , collagenase , elastase , cremaster muscle , chemistry , arteriole , vasodilation , extracellular , extracellular matrix , vasomotor , anatomy , vascular smooth muscle , bradykinin , microcirculation , endocrinology , medicine , biochemistry , pathology , smooth muscle , enzyme , receptor
The extracellular matrix contains a number of proteins including collagen and elastin. In addition to providing an extracellular scaffold, it is involved in physiological processes such as cell growth, differentiation, migration, and regulation of vasomotor tone. We hypothesized that breakdown of collagen or elastin in the intact vascular wall would cause arteriolar vasodilation. Rat cremaster 1A arterioles (n=29) were cannulated with glass micropipettes, pressurized, and warmed to 34°C. Internal diameter was monitored with an electronic video caliper. Exposure to type II collagenase (30 units/ml) for 5 min resulted in a transient 34.1±4.0% increase in diameter. Exposure to elastase (5 units/ml) for 5 min had no effect on diameter, but resulted in a 36.3±1.8% increase in length. Both collagenase and elastase treatments abolished myogenic responses, but preserved steady‐state dilation to acetylcholine and constriction to phenylephrine. Collagenase had no significant effect on vascular compliance, but elastase caused a significant leftward shift in the passive pressure/diameter curve. The results show that exposure of arterioles to collagenase resulted in transient vasodilation whereas elastase treatment caused irreversible lengthening of the vessel segment. These findings suggest differences in coupling of extracellular matrix proteins to vascular smooth muscle cells.