Arteries Stiffen With Age, but Can Retain an Ability to Become More Elastic With Applied External Cuff Pressure

It is accepted that arterial compliance decreases with age, with changes in the arterial pulse shape measured at the periphery. The aim of this study was to determine the relationship between arterial transmural pressure changes and changes in peripheral finger pulse shape characteristics for both older and younger subjects.Finger photoplethysmographic pulses were recorded noninvasively from the right index fingers of 100 healthy normotensive subjects. Their median age was 43 years (range 20-71 years) allowing two distinct age groups to be compared (older group ≥45 and younger group < 45 years). Arterial transmural pressures on the whole right arm were reduced with a 50 cm long cuff inflated to 10, 20, 30, and 40 mmHg. Pulse maximum amplitude and rise time were calculated for each age group, and for each cuff pressure level.Gradual and significant decreases in both pulse maximum amplitude and rise time were found with increasing cuff pressure for both age groups. With an external cuff pressure of 40 mmHg, there was an average maximum amplitude and rise time decrease of 27.1% (P < 0.001) and 7.5% (P < 0.001) respectively. The changes in the older group were significantly greater than those in the younger group for maximum amplitude (30.3% vs 24.4%, P = 0.006), but not for rise time (8.0% vs 6.7%, P = 0.23).Our results show that arterial compliance of the arm artery increases with reduced transmural pressure for both older and younger groups, and demonstrate that the aged arm artery can become more elastic with applied external cuff pressure

Impact of exercise training on arterial wall thickness in humans

Thickening of the carotid artery wall has been adopted as a surrogate marker of pre-clinical atherosclerosis, which is strongly related to increased cardiovascular risk. The cardioprotective effects of exercise training, including direct effects on vascular function and lumen dimension, have been consistently reported in asymptomatic subjects and those with cardiovascular risk factors and diseases. In the present review, we summarize evidence pertaining to the impact of exercise and physical activity on arterial wall remodelling of the carotid artery and peripheral arteries in the upper and lower limbs. We consider the potential role of exercise intensity, duration and modality in the context of putative mechanisms involved in wall remodelling, including haemodynamic forces. Finally, we discuss the impact of exercise training in terms of primary prevention of wall thickening in healthy subjects and remodelling of arteries in subjects with existing cardiovascular disease and risk factors

CCN2/Connective Tissue Growth Factor Is Essential for Pericyte Adhesion and Endothelial Basement Membrane Formation during Angiogenesis

CCN2/Connective Tissue Growth Factor (CTGF) is a matricellular protein that regulates cell adhesion, migration, and survival. CCN2 is best known for its ability to promote fibrosis by mediating the ability of transforming growth factor β (TGFβ) to induce excess extracellular matrix production. In addition to its role in pathological processes, CCN2 is required for chondrogenesis. CCN2 is also highly expressed during development in endothelial cells, suggesting a role in angiogenesis. The potential role of CCN2 in angiogenesis is unclear, however, as both pro- and anti-angiogenic effects have been reported. Here, through analysis of Ccn2-deficient mice, we show that CCN2 is required for stable association and retention of pericytes by endothelial cells. PDGF signaling and the establishment of the endothelial basement membrane are required for pericytes recruitment and retention. CCN2 induced PDGF-B expression in endothelial cells, and potentiated PDGF-B-mediated Akt signaling in mural (vascular smooth muscle/pericyte) cells. In addition, CCN2 induced the production of endothelial basement membrane components in vitro, and was required for their expression in vivo. Overall, these results highlight CCN2 as an essential mediator of vascular remodeling by regulating endothelial-pericyte interactions. Although most studies of CCN2 function have focused on effects of CCN2 overexpression on the interstitial extracellular matrix, the results presented here show that CCN2 is required for the normal production of vascular basement membranes