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Results for “Vascular Remodeling”

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At least 19 recordsLinked to original sources

PubMed2002

Angiotensin and cytoskeletal proteins: role in vascular remodeling.

Vascular remodeling occurs during normal development and is involved in various physiologic events. However, the adaptive structural changes of the vasculature can also be pathologic, leading to vascular disease such as hypertension, atherosclerosis, and vein graft disease. Pre-eclampsia may develop as a consequence of inappropriate vascular remodeling during pregnancy. Angiotensin II contributes to vascular remodeling by activating signal transduction cascades that promote vasoconstriction, growth, and inflammation. The cytoskeleton also participates in structural adaptation responses of the vasculature; cytoskeletal filaments may mediate vasoactive responses, transduce mechanical stimuli, and are involved in pharmacologic signal transduction. It has become clear that many of the cytoskeletal changes during vascular remodeling can be induced by angiotensin II. Recently, the small G-protein Rho has attracted much attention. The Rho/Rho-kinase system is activated by angiotensin II, is a prominent regulator of the cytoskeleton, and is involved in pathologic vascular remodeling.

Angiotensin II↗

PubMed2006

Genetic determinants of vascular remodelling.

Vascular remodelling is an important physiological mechanism that occurs as a result of changes in hemodynamics, and is a pathological process that plays a major role in the clinical manifestations of cardiovascular diseases. Using a mouse model, it was recently established that vascular remodelling is partially based on ligation of the carotid. In this model, low flow was associated with intima media thickening (IMT). IMT is a major manifestation of atherosclerosis of the carotid artery, and it is an important predictor of cardiovascular events. Carotid IMT has a strong genetic component. It was hypothesized that there would be genetically determined differences in outward remodelling and IMT induced by carotid flow alterations. Vascular remodelling among five inbred strains of mice were compared. Despite similar changes in flow in the left carotid among the strains, dramatic differences in remodelling of the partially ligated left carotid relative to control were observed. IMT correlated significantly with heart rate, outward remodelling and changes in plasminogen activator expression, cell proliferation and apoptosis. There were significant strain-dependent differences in the remodelling index (measured as the ratio of vessel area to IMT), which suggest fundamental alterations in sensing or transducing hemodynamic signals among strains. This model should be useful to identify and characterize the role of genes that mediate vascular remodelling.

Animals↗

PubMed1999

[Vasoactive substance and vascular remodeling].

Vascular remodeling is characterized by the dysfunction of endothelial cells, vascular smooth muscle cell (SMC) proliferation and migration, and the increased accumulation of extracellular matrix. Angiotensin II causes SMC growth and migration, and stimulates the expression of vascular remodeling-related genes. Angiotensin II activates a diversity of intracellular signal transduction cascades, and transactivation of epidermal growth factor and platelet-derived growth factor receptors via AT1 receptor seems to be responsible for the development of vascular remodeling. Not only angiotensin II but also endothelin-1, nitric oxide, c-type natriuretic peptide and adrenomedullin play an important role in the development of vascular remodeling.

Angiotensin II↗

PubMed2001

Plasmin and matrix metalloproteinases in vascular remodeling.

Vascular remodeling, defined as lasting structural changes in the vessel wall in response to hemodynamic stimuli, plays a role in many (patho)physiological processes requiring cell migration and degradation of extracellular matrix (ECM). Two proteolytic systems, the fibrinolytic (plasminogen/plasmin) and matrix metalloproteinase (MMP) systems can degrade most ECM components. The availability of mice models with deficiency of main components of both systems has allowed to study their contribution to vascular remodeling in several biological processes. In mouse models of atherosclerosis, urokinase-mediated plasmin generation plays a role in activation of several macrophage-derived MMPs (MMP-3, -9, -12 and -13), triggering elastolysis and collagenolysis, resulting in media destruction and aneurysm formation. Neointima formation after vascular injury, a process that depends on smooth muscle cell migration, is reduced in mice with plasminogen or urokinase deficiency and enhanced in mice with deficiency of TIMP-1 (type 1 tissue inhibitor of MMPs). Also in allograft transplant arteriosclerosis and in abdominal aortic aneurysm both proteolytic systems contribute to matrix degradation. In a mouse model of myocardial infarction, urokinase deficiency protects totally and MMP-9 deficiency partially against cardiac rupture, but these animals suffer cardiac failure. Thus, the plasminogen/plasmin and MMP systems, in concert, contribute to vascular remodeling in the setting of cardiovascular disease.

Animals↗

PubMed2003

Role of matrix metalloproteinases in vascular remodeling.

Vascular remodeling, defined as lasting structural changes in the vessel wall in response to hemodynamic stimuli, plays a role in many (patho)physiological processes requiring cell migration and degradation of extracellular matrix(ECM). Matrix metalloproteinase(MMP) system can degrade most ECM components. Several lines of evidence support a role for MMP system components in the development and progression of atherosclerosis and restenosis after angioplasty. This review article focuses on the role of MMPs in vascular remodeling relevant to atherosclerosis and restenosis after angioplasty.

Animals↗

PubMed1999

Review: Clinical aspects of vascular remodeling.

Vascular remodeling represents a spectrum of structural changes whereby the vascular wall responds to changes in its hemodynamic environment. Such changes may be classified as vessel enlargement (outward remodeling), diminution (inward remodeling), alternatively as adaptive (compensatory, appropriate to the hemodynamic stimulus), or maladaptive (dysfunctional, inappropriate). The direction and scale of remodeling are coordinated by endothelial production of growth factors, proteases, and cellular adhesion molecules in response to sensed changes in blood flow. In early atherosclerosis, outward remodeling preserves lumen size. Although protective in the long-term, the matrix degradation involved in this process may predispose atherosclerotic plaques to rupture, hence increasing the risks of acute coronary syndromes. Inward remodeling also occurs in advanced atherosclerotic lesions, whereby the vessel shrinks rather than enlarging, exacerbating rather than ameliorating stenosis. In transplant coronary artery disease, early inward remodeling may be a more important component of vessel stenosis than intimal thickening, while inappropriate inward remodeling appears to be as least as important as excessive intimal growth in the development of restenosis after angioplasty. Increased awareness of vascular remodeling, and in particular its malaptive forms, may provide new therapeutic insights for the future.

Animals↗

PubMed1996

Nitric oxide in vascular remodeling.

Vascular remodeling is a series of structural changes in blood vessels. Therefore, it may be conceivable that any humoral factors and physical forces acting on the vascular wall are involved in the remodeling processes. Cells in the vascular wall respond to the humoral and physical factors and may induce extracellular matrix, cell adhesion molecules and other humoral factors. They even grow so that cellular and noncellular components deviate from the normal population. We discuss the relationship among nitric oxide (NO), pressure and growth of smooth muscles. Decreased NO may be a consequence as well as a cause of high pressure. Similarly, high pressure is a cause as well as a consequence of decreased NO. Remodeling could be a consequence of both high pressure and decreased NO. Thus, vascular remodeling is a complex dynamic state, where any causes and results are influenced by each other. Interaction of NO and pressure is one such complexity.

Angiotensin II↗

PubMed2004

Olmesartan inhibits the expression of monocyte chemoattractant protein-1 and tumor necrosis factor-alpha and improves vascular remodeling after vascular injury in mouse.

OBJECTIVE: To investigate the neointima formation and the expression of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha) in cuff-induced vascular injury in mouse model, and to examine the effect of angiotensin II type 1 receptor (AT1) blocker, olmesartan, on MCP-1 and TNF-alpha expression and consequently vascular remodeling. METHODS: Vascular injury was induced by polyethylene cuff-placement around the mouse femoral artery. Some mice were treated with AT1 receptor blocker, olmesartan, at the dose of 3 mg.kg(-1).day(-1) with an osmotic minipump. Neointima formation and the proliferation of vascular smooth muscle cells (VSMCs) were measured by morphometric analysis and bromodeoxyuridine (BrdU) incorporation. MCP-1 and TNF-alpha expression was detected by Western blot and immunohistochemical staining. RESULTS: We observed neointima formation 14 days after cuff placement as well as VSMCs proliferation in the media and neointima. Cuff placement also induced MCP-1 and TNF-alpha expression in the media and neointima that the VSMCs specifically existed. Treatment of mice with olmesartan at a dose of 3 mg.kg(-1).day(-1), which did not influence systolic blood pressure, significantly decreased neointima formation and the proliferation of VSMCs. Olmesartan also inhibited MCP-1 and TNF-alpha expression in the injured arteries. CONCLUSIONS: Our results demonstrate that blockade of AT1 receptor inhibits MCP-1 and TNF-alpha expression and thereby improves vascular remodeling.

Analysis of Variance↗

PubMed2001

Coronary artery distensibility and compensatory vessel enlargement--a novel parameter influencing vascular remodeling?

Vascular remodeling implies the concept of compensatory vessel enlargement to preserve luminal dimensions during atheromatous plaque development. However, negative remodeling, i.e. vessel shrinkage in response to plaque accumulation has also been described. So far, the factors influencing positive or negative remodeling are uncertain. We hypothesized that vascular distensibility, a measure of vessel compliance, is related to compensatory enlargement. In 58 patients undergoing intravascular ultrasound interrogation of a de novo lesion prior to coronary intervention, the cross-sectional vessel area (VA), lumen area (LA) and plaque area (PA = VA minus LA) were measured at end diastole and end systole at the lesion site and at the proximal and distal reference segments. Positive remodeling was defined to be present when the VA at the lesion was > 1.05 times larger than that at the proximal reference (group A), negative remodeling when the VA at the lesion was < 0.95 of the reference site (group C) and in-between was considered to be intermediate (group B). Vessel compliance was measured by calculating vascular distensibility. Results showed a similar LA at the lesion site in all groups (4.18+/-2.18 vs. 4.36+/-1.19 vs. 3.74+/-1.81 mm2, NS) while VA and PA were significantly larger in group A (17.19+/-5.08 vs. 14.22+/-3.66 and 12.45+/-4.82 mm2, p = 0.005 and 13+/-4.55 vs. 9.95+/-3.58 and 8.7+/-3.83, p = 0.003, respectively). Vascular distensibility at the proximal reference segment was significantly greater in group A (3.55+/-2.67 vs. 1.25+/-1.03 and 0.85+/-0.73 mmHg(-1), p < 0.001) with a positive correlation between remodeling and distensibility (R = 0.52, p < 0.001). In a multiple regression model including clinical and lesional factors, distensibility was the only predictor of remodeling. In conclusion, these results suggest that compensatory vessel enlargement occurs to a greater degree in patients with increased coronary artery distensibility, which appears to be a predictor for positive remodeling.

Adaptation, Physiological↗

PubMed1997

[Vascular "remodeling"].

Vascular remodeling means a specific organization of the vascular wall around a diminished lumen as to the before existing conditions, with consequent vascular geometry modification. This organization comes from the response of all vascular components (endothelium, muscular cells, connective component, etc.) to physical and chemical stimuli. Particular behaviour of the vascular wall has lately been pointed out, both in long known pathologies (arteriosclerosis, arterial hypertension, diabetes mellitus, arteriosclerotic aneurysms) and in situations involving both physiopathology (ischaemia-reperfusion, angiogenesis) as therapy (angioplasty).

Aneurysm↗

PubMed1994

Antagonism between the vascular renin-angiotensin and natriuretic peptide systems in vascular remodelling.

Vascular remodelling is central to the pathophysiology of hypertension and atherosclerosis. Recent evidence suggests the pivotal role of vasoactive substances occurring in the blood vessel, such as angiotensin II (AII), in the control of vascular growth. We recently discovered that C-type natriuretic peptide (CNP), the third member of the natriuretic peptide family, is produced by vascular endothelial cells and can act as an endothelium-derived relaxing peptide. We also demonstrated gene expression of CNP and the ANP-B receptor, which is one of the three subtypes of the natriuretic peptide receptor and is specific to CNP in blood vessels in vivo. Thus, we propose the existence of a "vascular natriuretic peptide system (NPS)" similar to the vascular renin-angiotensin system (RAS). The present study showed that CNP exerted a growth-inhibitory action and antagonised the growth-promoting action of AII, which was mediated through the AII subtype 1 receptor in cultured vascular smooth muscle cells. In neointimal lesions of rat carotid artery, CNP gene transcript was detectable 2 weeks after balloon injury, and ANP-B receptor gene expression was augmented. These findings suggest that the vascular NPS is activated in proliferative vascular lesions, suppressing further proliferation by antagonising the action of the vascular RAS.

Angiotensin II↗

PubMed2006

Effect of traditional Chinese medicine Qin-Dan-Jiang-Ya-Tang on remodeled vascular phenotype and osteopontin in spontaneous hypertensive rats.

Qin-Dan-Jiang-Ya-Tang (QDJYT) is a traditional Chinese herbal medicine for the treatment of hypertension. The effect of QDJYT on blood pressure and on vascular remodeling in hypertension was investigated in the model of spontaneous hypertensive rats (SHR). Sixteen SHRs were divided into two groups, the SHR group and the SHR+QDJYT group. Eight WKY rats were a normal control group. QDJYT (750 mg/kg) was orally administered daily for 12 weeks in SHR+QDJYT group. After 12 weeks, thoracic aortas were segregated. Media thickness (MT), lumen diameter (LD), the ratio of MT to LD, the volume fraction of collagen (VFC) in media, the ultrastructure of vascular smooth muscle cells (VSMCs) and the expression of osteopontin (OPN) mRNA were examined by histological staining, transmission electron microscope (TEM), and real-time PCR, respectively. It was observed in our study that MT, MT/LD, VFC and the expression of OPN mRNA were higher in the SHRs than in the WKY rats, volume and numeral density of mitochondria in vascular smooth muscle cells (VSMCs) in media increased obviously. However, in the SHRs treated with QDJYT, we found MT, MT/LD, VFC and the expression of OPN gene were lower than in the SHRs, and the phenotype of VSMCs were close to normal. These results suggest that QDJYT could reverse the vascular remodeling in SHR, and the mechanisms may be related to the suppressive effect of QDJYT on the expression of OPN mRNA in arterial wall.

Anti-Infective Agents↗

PubMed2004

CXCL11 attenuates bleomycin-induced pulmonary fibrosis via inhibition of vascular remodeling.

Aberrant vascular remodeling is a central hallmark for the development and progression of idiopathic pulmonary fibrosis. The mechanisms underlying the pathophysiologic alterations, however, are poorly understood. A recent phase II trial of interferon gamma-1b has demonstrated a trend toward a decrease in profibrotic and proangiogenic biologic markers, and upregulation of lung CXCL11 mRNA and bronchoalveolar lavage fluid and plasma protein levels of CXCL11. We hypothesized that net aberrant vascular remodeling seen during the pathogenesis of fibroplasia and deposition of extracellular matrix during bleomycin-induced pulmonary fibrosis can be attenuated by treatment with the angiostatic ELR(-) CXC chemokine, CXCL11. In a preclinical model, systemic administration of CXCL11 reduced pulmonary collagen deposition, procollagen gene expression, and histopathologic fibroplasia and extracellular matrix deposition in the lung of bleomycin-treated mice. CXCL11 treatment significantly reduced bleomycin-induced pulmonary fibrosis without altering specific lung leukocyte populations. CXCR3 is not expressed on fibroblasts and CXCL11 had no direct functional effect on pulmonary fibroblasts. The angiogenic activity in the lung was significantly decreased, however, and CXCL11 treatment reduced the total number of endothelial cells in the lung following bleomycin exposure. The results suggest that CXCL11 inhibits pulmonary fibrosis by altering aberrant vascular remodeling.

Angiogenesis Inhibitors↗

PubMed1998

Direct evidence for the importance of endothelium-derived nitric oxide in vascular remodeling.

The vascular endothelium mediates the ability of blood vessels to alter their architecture in response to hemodynamic changes; however, the specific endothelial-derived factors that are responsible for vascular remodeling are poorly understood. Here we show that endothelial-derived nitric oxide (NO) is a major endothelial-derived mediator controlling vascular remodeling. In response to external carotid artery ligation, mice with targeted disruption of the endothelial nitric oxide synthase gene (eNOS) did not remodel their ipsilateral common carotid arteries whereas wild-type mice did. Rather, the eNOS mutant mice displayed a paradoxical increase in wall thickness accompanied by a hyperplastic response of the arterial wall. These findings demonstrate a critical role for endogenous NO as a negative regulator of vascular smooth muscle proliferation in response to a remodeling stimulus. Furthermore, our data suggests that a primary defect in the NOS/NO pathway can promote abnormal remodeling and may facilitate pathological changes in vessel wall morphology associated with complex diseases such as hypertension and atherosclerosis.

Adaptation, Physiological↗

PubMed2006

Intracranial aneurysms: links among inflammation, hemodynamics and vascular remodeling.

Abnormal vascular remodeling mediated by inflammatory cells has been identified as a key pathologic component of various vascular diseases, including abdominal aortic aneurysms, brain arteriovenous malformations and atherosclerosis. Based on findings from observational studies that analysed human intracranial aneurysms and experimental studies that utilized animal models, an emerging concept suggests that a key component of the pathophysiology of intracranial aneurysms is sustained abnormal vascular remodeling coupled with inflammation. This concept may provide a new treatment strategy to utilize agents to inhibit inflammation or cytokines produced by inflammatory cells such as matrix metalloproteinases. Such an approach would aim to stabilize these vascular lesions and prevent future expansion or rupture.

Animals↗

PubMed2001

Rationale and design for the SARIS trial; effect of statin on atherosclerosis and vascular remodeling assessed with intravascular sonography. Effect of Statin on Atherosclerosis and vascular Remodeling assessed with Intravascular Sonography.

PURPOSE: The SARIS study (effect of Statin on Atherosclerosis and vascular Remodeling assessed with Intravascular Sonography) is a prospective randomized multicenter trial designed to assess both morphological and functional cardiovascular effects of atorvastatin. METHODS: Participating centers will include 50 patients with normal to mildly elevated cholesterol levels eligible for balloon angioplasty and/or stent placement of the common iliac artery. Patients will be randomized to 1-year treatment with either low-dose (10 mg) or high-dose (80 mg) atorvastatin. The morphological effects of atorvastatin will be studied using intravascular ultrasound (IVUS); the effect of atorvastatin on both plaque volume and vascular remodeling seen at 1-year follow-up will be investigated. The functional cardiovascular effects of atorvastatin will be studied using dobutamine stress echocardiography (DSE); the effect of atorvastatin on myocardial coronary flow reserve at 6-months and 1-year follow-up will be investigated. The aims of the present study are noteworthy in respect that (1) IVUS is the only available technique to sensitively measure the effect of atorvastatin on both intimal hyperplasia and vascular remodeling, and (2) DSE is a non-invasive test to objectively quantify the effect of atorvastatin on the functionality of the coronary artery.

Anticholesteremic Agents↗

PubMed1999

[Role of L-arginine--endogenous NOS inhibitors--endothelin-1 pathway for the vascular remodelling].

Mechanisms of vascular remodelling process are complex and poorly understood. We describe herein the role of L-arginine-endogenous NOS inhibitors-endothelin-1 pathway for the vascular remodelling after endothelial denudation of the rabbit carotid artery. It is reportedly known that NO is a vasodilating substance, an inhibitor of platelet aggregation and adhesion, and an inhibitor of vascular smooth muscle cell proliferation and that endothelin-1, of which production is inhibited by NO, is a potent vasoconstrictor and a potent mitogen. An accumulation of endogenous inhibitors (L-NMMA and ADMA) in regenerated endothelial cells after the endothelial denudation was accompanied by the decreased NO generation, the increased endothelin-1 content within the vessel wall and the occurrence of intimal hyperplasia. Endothelin-1 content within the vessel wall was significantly increased after the exogenous L-NMMA administration for 2 weeks, suggesting that accumulated L-NMMA results in the decreased NO generation and, in turn, increases endothelin-1 content. Endothelin-1 facilitated the [3H]-L-NMMA uptake by endothelial cell and brought about the potentiation of L-NMMA-mediated inhibition of NO generation. These results strongly suggest that the L-arginine--endogenous NOS inhibitors--endothelin-1 pathway plays an active role for vascular remodelling.

Animals↗

PubMed2000

Anti-monocyte chemoattractant protein-1 gene therapy inhibits vascular remodeling in rats: blockade of MCP-1 activity after intramuscular transfer of a mutant gene inhibits vascular remodeling induced by chronic blockade of NO synthesis.

Monocyte chemoattractant protein-1 (MCP-1) may play an essential part in the formation of arteriosclerosis by recruiting monocytes into the arterial wall. Thus, we devised a new strategy for anti-MCP-1 gene therapy against arteriosclerosis by transfecting an amino-terminal deletion mutant (missing the amino-terminal amino acids 2 to 8) of the human MCP-1 gene into a remote organ (skeletal muscles). Intramuscular transduction with the mutant MCP-1 gene blocked monocyte recruitment induced by a subcutaneous injection of recombinant MCP-1. In a rat model in which the chronic inhibition of endothelial nitric oxide synthesis induces early vascular inflammation as well as subsequent coronary vascular remodeling, this strategy suppressed monocyte recruitment into the coronary vessels and the development of vascular medial thickening, but did not reduce perivascular fibrosis. Thus, MCP-1 is necessary for the development of medial thickening but not for fibrosis in this model. This new strategy may be a useful and feasible gene therapy against arteriosclerosis.

Animals↗