April 1, 1997Circulation
Different Effects of Thrombin Receptor Activation on Endothelium and Smooth Muscle Cells of Human Coronary Bypass Vessels
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Discussion
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Implication
Ex vivo study reveals distinct thrombin responses in internal mammary arteries versus saphenous veins, highlighting mechanisms underlying coronary bypass graft disease.
Key Points
- Investigate the differential effects of thrombin receptor activation on vascular tone and smooth muscle cell proliferation in human internal mammary arteries and saphenous veins.
- Measured isometric tension changes in isolated human internal mammary artery and saphenous vein rings treated with thrombin, thrombin receptor agonist peptide, and thrombin inhibitors.
- Quantified smooth muscle cell proliferation via [3H]thymidine incorporation and evaluated p42MAPK activation in cultured cells.
- Assessed thrombin receptor expression in endothelial and smooth muscle layers using reverse transcription polymerase chain reaction and immunohistology.
- Thrombin induced endothelium-dependent relaxation (65 ± 5%) in internal mammary arteries, which was reproduced by receptor agonist peptide and inhibited by r-hirudin or PPACK (P < .05).
- Thrombin stimulated contractions in saphenous veins (36 ± 5% of 100 mmol/L KCl, P < .05) that were blocked by thrombin inhibitors but not reproduced by receptor agonist peptide.
- Smooth muscle cells from saphenous veins displayed significantly greater thrombin-induced [3H]thymidine incorporation than internal mammary artery cells (P < .05), despite comparable p42MAPK activation.
Cite This Study
Yang et al. (1997) studied this question.