Matrix metalloproteinase 2–induced venous dilation via hyperpolarization and activation of K+ channels: Relevance to varicose vein formation Joseph D.

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Matrix metalloproteinase 2–induced venous dilation via hyperpolarization and activation of K+ channels: Relevance to varicose vein formation Joseph D. Raffetto, MD, Reagan L. Ross, BS, MPT, Raouf A. Khalil, MD, PhD Journal of Vascular Surgery Volume 45, Issue 2, Pages 373-380 (February 2007) DOI: 10.1016/j.jvs.2006.10.041 Copyright © 2007 The Society for Vascular Surgery Terms and Conditions

Fig 1 Matrix metalloproteinase (MMP)-2–induced relaxation of phenylephrine (Phe) contraction in endothelium-intact inferior vena cava (IVC) segments not treated (A) or pretreated with NG-l-nitro-arginine methyl ester (l-NAME; 10−4 mol/L) (B) or l-NAME plus indomethacin (10−5 mol/L) (C) or endothelium-denuded IVC segments (D). When Phe (10−5 mol/L) reached a steady state, MMP-2 (1 μg/mL) was added, and its effect on Phe contraction was observed. The traces are representative of three to five experiments. -Endo, endothelium-denuded segments. Journal of Vascular Surgery 2007 45, 373-380DOI: (10.1016/j.jvs.2006.10.041) Copyright © 2007 The Society for Vascular Surgery Terms and Conditions

Fig 2 Aggregate data evaluating the effect of matrix metalloproteinase (MMP)-2 on phenylephrine (Phe) contraction in endothelium-intact inferior vena cava (IVC) segments not treated or treated with NG-l-nitro-arginine methyl ester (l-NAME) and indomethacin and in endothelium-denuded segments (-endo). Data represent the mean ± SEM of measurements in three to five experiments. *P < .05 compared with control experiments in endothelium-intact tissues and experiments in endothelium-blocked tissues. Journal of Vascular Surgery 2007 45, 373-380DOI: (10.1016/j.jvs.2006.10.041) Copyright © 2007 The Society for Vascular Surgery Terms and Conditions

Fig 3 Effect of matrix metalloproteinase (MMP)-2 on nitrite/nitrate production as measured by Griess reagent (A) and on nitric oxide (NO) production as measured by 4-amino-5-methylamino-2′,7′-difluorescein (DAF) fluorescence (B). Basal, MMP-2, and acetylcholine (ACh)-induced NO production were measured. Data represent the mean ± SEM of measurements in three experiments. Journal of Vascular Surgery 2007 45, 373-380DOI: (10.1016/j.jvs.2006.10.041) Copyright © 2007 The Society for Vascular Surgery Terms and Conditions

Fig 4 Effects of matrix metalloproteinase (MMP)-2 during membrane depolarization by KCl, a condition that does not favor K+ efflux and cell hyperpolarization. High KCl (96 mmol/L) contraction was elicited, MMP-2 (1 μg/mL) was added, and its lack of effect was observed. Data represent the mean ± SEM. Journal of Vascular Surgery 2007 45, 373-380DOI: (10.1016/j.jvs.2006.10.041) Copyright © 2007 The Society for Vascular Surgery Terms and Conditions

Fig 5 Effect of cromakalim on matrix metalloproteinase (MMP)-2–induced inferior vena cava (IVC) relaxation. IVC contraction to phenylephrine (Phe) was elicited. Control tissue (upper panel) was treated with vehicle Krebs solution. In other tissues (lower panel), cromakalim (10−7 mol/L) was added, and IVC relaxation was observed. MMP-2 was then added, and further IVC relaxation to baseline could be observed. Journal of Vascular Surgery 2007 45, 373-380DOI: (10.1016/j.jvs.2006.10.041) Copyright © 2007 The Society for Vascular Surgery Terms and Conditions

Fig 6 Effect of iberiotoxin on matrix metalloproteinase (MMP)-2–induced inferior vena cava (IVC) relaxation. IVC contraction to phenylephrine (Phe) was elicited. Control tissue (top panel) was treated with vehicle Krebs solution. In other tissues (middle panel), the addition of iberiotoxin (a BKCa blocker) prevented MMP-2–induced relaxation of Phe-contracted IVC. The cumulative effects of MMP-2 in the absence or presence of iberiotoxin are presented in the bottom panel. *P < .05. Journal of Vascular Surgery 2007 45, 373-380DOI: (10.1016/j.jvs.2006.10.041) Copyright © 2007 The Society for Vascular Surgery Terms and Conditions