Key result
Experimentally reduced compliance in porcine carotid arteries decreased norepinephrine-induced contraction capacity and altered protein expressions associated with matrix degradation and proliferation.
Why the study?
Does reduced cyclic stretch alter vascular smooth muscle cell function and remodeling in porcine carotid arteries?
Does reduced cyclic stretch alter vascular smooth muscle cell function and remodeling in porcine carotid arteries?
Reduced cyclic stretch in ex vivo porcine carotid arteries impairs smooth muscle cell contractile function and promotes matrix degradation and cellular proliferation.
May impair VSMC contractility in low-compliance arteries; leaves open whether cyclic stretch modulates human vascular remodeling.
BACKGROUND: With advancing age arteries stiffen, reducing arterial compliance and leading to the development of systolic hypertension and to a substantial increase in pulse pressure. An augmented pulse pressure can be a predictor of the development of hypertension, which has been linked to several cardiovascular diseases including atherosclerosis, and to pathologies such as diabetes and renal dysfunction. In this study, we tested the hypothesis that reduced wall compliance induces pulse-pressure-mediated changes in arterial wall metabolism and remodeling. METHODS: Porcine carotid arteries were perfused for 24 h using an ex vivo arterial support system. Control arteries were exposed to a pulse shear stress (6 +/- 3 dynes/cm(2)) combined with a pulse pressure of 80 +/- 10 mm Hg, yielding a physiological cyclic stretch of 4-5%. A reduced compliance group was also studied, in which arteries were wrapped with an external band, thereby decreasing cyclic stretch to levels <1%. RESULTS: The experimentally reduced compliance caused a decreased contraction capacity induced by norepinephrine(NE), and this was associated with lower levels of alpha-smooth muscle cell-actin (alpha-SMC-actin) and desmin protein expressions. Arteries that were exposed to a reduced cyclic stretch exhibited a higher level of matrix metalloproteinase-2 (MMP-2) expression activity as well as an increase in Ki67 expression, thereby suggesting that matrix degradation and cellular proliferation had been initiated. Furthermore, the expression of plasminogen activator inhibitor-1 (PAI-1) in stiffened arteries was lower than in the control arteries. CONCLUSIONS: These findings underline the importance of cyclic stretch in the maintenance of a differentiated and fully functional phenotype of vascular SMCs, as well as in the regulation of migratory properties, proliferation, and matrix turnover.
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Gambillara et al. (2008) studied Arterial stiffness. Reduced compliance (external band decreasing cyclic stretch to <1%) vs. Control arteries exposed to physiological cyclic stretch of 4-5% was evaluated on Arterial wall metabolism and remodeling (contraction capacity and protein expressions). Experimentally reduced compliance in porcine carotid arteries decreased norepinephrine-induced contraction capacity and altered protein expressions associated with matrix degradation and proliferation.
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