Abstract

The concept that blood pressure influences vessel wall composition and structure is well established. Any alterations in stretch (caused by changes in blood pressure) solicit counteracting radial and tangential forces, driving transformations in the vessel wall that aim to accommodate the new conditions and to ultimately restore basal levels of tensile stress.1–3 Thus, when tensile stress increases because of a rise in arterial pressure, smooth muscle cell hypertrophy and collagen and elastin contents augment. Inversely, when the circumferential stress falls, the wall undergoes atrophy.4,5 See page 957 Understanding how vessel wall remodeling occurs is valuable because it relies on the delicate balance between restructuralization and overcompensation. For instance, vascular accumulation of type I, III, and IV collagen in hypertensive patients6 and in animal models of hypertension7,8 effectively counteracts the distending force of blood pressure, but at length it also results in increased vascular stiffness. Clinically, vascular stiffness translates to greater pulse wave velocity, which is an independent predictor of mortality in patients with end-stage renal failure, hypertension, and diabetes, as well as in older individuals.9 In this issue of Atherosclerosis, Thrombosis and Vascular Biology , Jackson et al10 show that the opposite holds true for vessels in which axial tension is off-loaded. In rabbit carotid arteries elongated by interposition of the contralateral carotid artery, the authors found that tortuosity caused by loss of axial strain was not rectified in the months that followed the intervention. Smooth muscle cell proliferation was observed, but this was offset by equivalent cell apoptosis. Likewise, elastin and collagen accumulation was countered by matrix metalloproteinase (MMP) upregulation and activation. But on close observation of the extracellular matrix (ECM), it became apparent that the fenestrae of the internal elastic laminae were greatly enlarged, and indeed the authors found that …

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call