Arterial expansive remodeling induced by high flow rates

Driss, Ahmed Ben; Bénessiano, Joëlle; Poitevin, Pierre; Lévy, Bernard; Michel, Jean‐Baptiste

doi:10.1152/ajpheart.1997.272.2.h851

Cited by 122 publications

(132 citation statements)

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“…In animal models, creation of an aortocaval shunt is associated with a marked increase in aortic flow and shear stress followed by a progressive increase in aortic diameter, which tends to restore aortic shear stress to control levels. 14 Similarly, in our study participants, higher body weight, which is associated with increased resting cardiac output, was associated with increased aortic diameter. Thus, experimental models and data from humans suggest that aortic diameter is actively modulated in response to physiological stimuli.…”

Section: Discussionsupporting

confidence: 71%

Aortic Diameter, Wall Stiffness, and Wave Reflection in Systolic Hypertension

Mitchell¹,

Conlin

Dunlap³

et al. 2008

Hypertension

159

119

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Abstract-Systolic hypertension is associated with increased pulse pressure (PP) and increased risk for adverse cardiovascular outcomes. However the pathogenesis of increased PP remains controversial. One hypothesis suggests that aortic dilatation, wall stiffening and increased pulse wave velocity result from elastin fragmentation, leading to a premature reflected pressure wave that contributes to elevated PP. An alternative hypothesis suggests that increased proximal aortic stiffness and reduced aortic diameter leads to mismatch between pressure and flow, giving rise to an increased forward pressure wave and increased PP. To evaluate these two hypotheses, we measured pulsatile hemodynamics and proximal aortic diameter directly using tonometry, ultrasound imaging, and Doppler in 167 individuals with systolic hypertension. Antihypertensive medications were withdrawn for at least 1 week before study. Key Words: hypertension Ⅲ hemodynamics Ⅲ pulse pressure Ⅲ aorta Ⅲ vascular stiffness Ⅲ pulse wave velocity T he strong relation between pulse pressure (PP) and cardiovascular events, and the importance of elevated PP in the pathogenesis of systolic hypertension, has stimulated considerable interest in establishing potential mechanisms of increased PP. Early studies focused on the importance of medial degeneration in the aorta as the principal mechanism for the increase in PP that accompanies aging. 1 One hypothesis asserts that mechanical fatigue and fragmentation of the elastin fibers of the aorta leads to dilatation of the proximal aorta and transfers load to stiffer elements of the aortic wall, such as collagen. As a result, aortic wall stiffness and pulse wave velocity (PWV) increase, resulting in premature arrival of reflected pressure waves from the periphery. According to this hypothesis, premature arrival of the reflected pressure wave during systole is considered to be the primary mechanism contributing to increased PP and development of systolic hypertension. 1 For this hypothesis to be correct, PP should be related closely to the extent of pressure augmentation in the central aorta (augmentation index). Furthermore, elevated PP should be associated with increased aortic diameter and PWV.We recently reported that characteristic impedance (Z c ), which is a measure of the pressure-flow relation of the proximal aorta, was elevated out of proportion to the increase in carotid-femoral PWV in individuals with systolic hypertension. 2 Z c is proportional to local PWV divided by local cross-sectional area. Therefore, we proposed that the observed pattern of a predominant increase in Z c with only a moderate increase in carotid-femoral PWV in individuals with a wide PP suggested a reduction in aortic diameter. In this setting the primary mechanism for increased PP would be the mismatch between aortic flow and diameter leading to increased forward wave amplitude, rather than premature wave reflection. To further assess the validity of these alternative hypotheses, we studied pulsatile hemodynamics and aortic root diam...

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Section: Discussionsupporting

confidence: 71%

Aortic Diameter, Wall Stiffness, and Wave Reflection in Systolic Hypertension

Mitchell¹,

Conlin

Dunlap³

et al. 2008

Hypertension

159

119

View full text Add to dashboard Cite

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“…Similarly, several groups have reported that increased arterial flow elicits an increase of endothelium-derived vascular NO and cGMP levels. 6,50,51 Thus, NO-stimulated cell migration could serve as a wound-repair mechanism or it could also be involved in vascular remodeling that has been shown to occur in the presence of altered arterial flow. 6 A similar role can also be attributed to CNP on the basis of its existence in endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Nitric Oxide and C-Type Atrial Natriuretic Peptide Stimulate Primary Aortic Smooth Muscle Cell Migration via a cGMP-Dependent Mechanism

Brown

Pan

Hassid

1999

Circulation Research

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Abstract-Migration of aortic smooth muscle cells is thought to be of essential importance in vascular restenosis, remodeling, and angiogenesis. Recent studies have shown that NO donors inhibit the migration of subcultured aortic smooth muscle cells. However, there is evidence that NO elicits opposite effects on cell proliferation in primary versus subcultured cells, indicating fundamental differences among different models of aortic smooth muscle cell cultures. The purpose of the current study was to investigate the effect of NO donors on migration of primary cultures of rat aortic smooth muscle cells and to compare and contrast their response with those in subcultured cells. A second purpose was to investigate some of the underlying mechanisms associated with NO-induced effects on cell migration. We report that 2 NO donors, S-nitroso-N-acetylpenicillamine (SNAP) and 2,2-(hydroxynitrosohydrazino)bis-ethanamine, stimulated the migration of primary cells in a wounded-culture model as well as in a transwell migration model. The effect of NO donors was mimicked by 2 cGMP analogues and C-type natriuretic peptide and blocked by a specific inhibitor of guanyl cyclase, 1H-(1,2,4)oxadiazolo[4,3,-a]quinoxalin-1-one, indicating the involvement of cGMP as second messenger. Moreover, neither NO donors nor cGMP analogues altered migration of primary cultures stimulated by either FBS or angiotensin II. In contrast to its effect in primary cultures, SNAP did not alter basal or stimulated migration of subcultured cells, except at a relatively high concentration of 1 mmol/L, at which migration was inhibited. The migration-stimulatory effect of NO donors and cGMP was associated with altered cell morphology and dissociation of actin filaments, consistent with recent studies indicating that cell morphology and cytoskeletal organization influence cell migration. The results suggest the possible involvement of NO-induced cell migration in vascular injury or remodeling, representing conditions in which vascular NO levels would be expected to be elevated. (Circ Res. 1999;84:655-667.)

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“…First, the low-resistance circuit resulting from creation of the AV anastomosis triggers an immediate increase in blood flow and wall shear stress (WSS) through the inflow artery (5)(6)(7). Second, these rapid increases in arterial blood flow and WSS stimulate an endothelium-dependent vasodilatory response in the artery and vein, mediated largely by nitric oxide (NO) and activation of matrix metalloproteinases (MMPs), that dilates both the inflow artery and outflow vein, restores WSS toward baseline, and inhibits neointimal hyperplasia development (7)(8)(9)(10)(11). Appropriate upregulation of MMPs results in matrix degradation and restructuring of the vascular scaffold, leading to luminal expansion (9,11,12).…”

Section: Vascular Remodeling and Neointimal Hyperplasia Developmentmentioning

confidence: 99%

New Insights into Dialysis Vascular Access: Molecular Targets in Arteriovenous Fistula and Arteriovenous Graft Failure and Their Potential to Improve Vascular Access Outcomes

Lee

Misra

2016

CJASN

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Vascular access dysfunction remains a major cause of morbidity and mortality in hemodialysis patients. At present there are few effective therapies for this clinical problem. The poor understanding of the pathobiology that leads to arteriovenous fistula (AVF) and graft (AVG) dysfunction remains a critical barrier to development of novel and effective therapies. However, in recent years we have made substantial progress in our understanding of the mechanisms of vascular access dysfunction. This article presents recent advances and new insights into the pathobiology of AVF and AVG dysfunction and highlights potential therapeutic targets to improve vascular access outcomes.

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Arterial expansive remodeling induced by high flow rates

Cited by 122 publications

References 0 publications

Aortic Diameter, Wall Stiffness, and Wave Reflection in Systolic Hypertension

Aortic Diameter, Wall Stiffness, and Wave Reflection in Systolic Hypertension

Nitric Oxide and C-Type Atrial Natriuretic Peptide Stimulate Primary Aortic Smooth Muscle Cell Migration via a cGMP-Dependent Mechanism

New Insights into Dialysis Vascular Access: Molecular Targets in Arteriovenous Fistula and Arteriovenous Graft Failure and Their Potential to Improve Vascular Access Outcomes

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