Interaction of transmural pressure and shear stress in the transport of albumin across the rabbit aortic wall

Karmakar, Nivedita

doi:10.1016/s0021-9150(00)00688-2

Cited by 9 publications

(14 citation statements)

References 25 publications

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“…We did not study the impact of blood flow on the effects of IS. In vivo, vascular endothelial cells are constantly exposed to shear stress as a result of blood flow, and shear stresses have been shown to affect endothelial barrier function [Karmakar, 2001;Ogunrinade et al, 2002]. Another study also reported that, after exposed to disturbed flow, discontinuous VE-cadherin staining on BPAECs and the presence of gaps in the intercellular junction were demonstrated [Miao et al, 2005].…”

Section: Discussionmentioning

confidence: 98%

Effects of indoxyl sulfate on adherens junctions of endothelial cells and the underlying signaling mechanism

Peng

Lin

Chen

et al. 2012

J of Cellular Biochemistry

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Uremic patients have a much higher risk of cardiovascular diseases and death. Uremic toxins are probably involved in the development of vascular endothelial dysfunction. Indoxyl sulfate (IS) is a uremic toxin that accumulates with deterioration of renal function. This study explored the effects of IS on the adherens junctions of vascular endothelial cells and revealed the underlying mechanism. Bovine pulmonary artery endothelial cells (BPAECs) were treated with IS, and the distribution of vascular endothelial cadherin (VE-cadherin), p120-catenin, β-catenin, and stress fibers was examined by immunofluorescence. IS treatment resulted in disruption of intercellular contacts between BPAECs with prominent parallel-oriented intracellular stress fiber formation. Intracellular free radical levels which measured by flow cytometry increased after IS treatment. The antioxidant, MnTMPyP, and an ERK pathway inhibitor, U0126, both significantly prevented IS-induced disruption of intercellular contacts. Western blotting analyses demonstrated that IS-induced phosphorylation of myosin light chain kinase (MLCK) and myosin light chains (MLC) as well as activation of extracellular-signal-regulated protein kinase (ERK1/ERK2). Pretreatment with MnTMPyP prevented ERK1/2 phosphorylation. U0126 prevented the IS-induced MLCK and MLC phosphorylation. MEK-ERK acted as the upstream regulator of the MLCK-MLC pathway. These findings suggest that the superoxide anion-MEK-ERK-MLCK-MLC signaling mediates IS-induced junctional dispersal of BPAECs.

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Section: Discussionmentioning

confidence: 98%

Effects of indoxyl sulfate on adherens junctions of endothelial cells and the underlying signaling mechanism

Peng

Lin

Chen

et al. 2012

J of Cellular Biochemistry

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“…[18][19][20][21][22][23][24][25] It is synthesized in cells from L-arginine to L-citrulline via activation of a calciumdependent nitric oxide synthase. In response to platelet-derived products, hormones and mechanical changes such as transmural pressure, 26 endothelial cells release NO into the surrounding milieu. NO enters smooth muscle cells and activates soluble guanylate cyclase.…”

Section: Endothelium-derived Relaxing Factorsmentioning

confidence: 99%

The pathogenesis of diabetic retinopathy: old concepts and new questions

Cai

Boulton

2002

Eye

291

196

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Hyperglycaemia appears to be a critical factor in the aetiology of diabetic retinopathy and initiates downstream events including: basement membrane thickening, pericyte drop out and retinal capillary non-perfusion. More recently, focus has been directed to the molecular basis of the disease process in diabetic retinopathy. Of particular importance in the development and progression of diabetic retinopathy is the role of growth factors (eg vascular endothelial growth factor, placenta growth factor and pigment epithelium-derived factor) together with specific receptors and obligate components of the signal transduction pathway needed to support them. Despite these advances there are still a number of important questions that remain to be answered before we can confidently target pathological signals. How does hyperglycaemia regulate retinal vessels? Which growth factors are most important and at what stage of retinopathy do they operate? What is the preferred point in the growth factor signalling cascade for therapeutic intervention? Answers to these questions will provide the basis for new therapeutic interventions in a debilitating ocular condition.

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“…Several studies have shown that transvascular exchange can be affected by a change in perfusion rate (14,17,19,32,33,43). A small-pore model has been proposed as a possible mechanism to account for flow-dependent transport of small solutes in cannulated vessels (32); moreover, there have been several recent studies of shearinduced increases in fluid filtration performed in vitro (3, 6, 37) and in vivo (27,40,41).…”

mentioning

confidence: 99%

Regulation of capillary hydraulic conductivity in response to an acute change in shear

Kim¹,

Harris²,

Tarbell³

2005

American Journal of Physiology-Heart and Circulatory Physiology

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-The effects of mechanical perturbations (shear stress, pressure) on microvascular permeability primarily have been examined in micropipette-cannulated vessels or in endothelial monolayers in vitro. The objective of this study is to determine whether acute changes in blood flow shear stress might influence measurements of hydraulic conductivity (Lp) in autoperfused microvessels in vivo. Rat mesenteric microvessels were observed via intravital microscopy. Occlusion of a third-order arteriole with a micropipette was used to divert and increase flow through a nonoccluded capillary or fourth-order arteriolar branch. Using the micropipette occlusion technique in autoperfused rather than cannulated capillaries, Landis described how the fluid filtration rate was most rapid in the initial seconds following occlusion, becoming significantly slower in less than 1 min. This was attributed at least in part to the possibility that plasma oncotic pressure could increase with time in an occluded vessel as a result of greater efflux of water than of protein. However, another consideration is that the vessel occlusion includes an abrupt change in flow-induced shear stress and pressure, both of which could have a time-dependent effect on L p .As a microvessel is occluded, blood flow decreases from its basal value to essentially zero. Several studies have shown that transvascular exchange can be affected by a change in perfusion rate (14,17,19,32,33,43). A small-pore model has been proposed as a possible mechanism to account for flow-dependent transport of small solutes in cannulated vessels (32); moreover, there have been several recent studies of shearinduced increases in fluid filtration performed in vitro (3, 6, 37) and in vivo (27,40,41). The mechanism by which shear forces could increase L p appear to be dependent on nitric oxide (NO) (3,15,24). Therefore, when a capillary stops flowing, it might be expected that L p could decline in a matter of seconds as shear-induced production of NO is attenuated.Another mechanical factor associated with microvessel occlusion is the step increase in hydrostatic pressure. For example, when a capillary is occluded at its downstream end, pressure throughout the vessel increases to that of the feeding arteriole. Recent studies (7,38) indicate that a step increase in hydrostatic pressure causes a decrease in L p in what has been called a "sealing effect." However, the time courses of the changes in L p in these studies were over a period of minutes to hours.The effects of shear on L p have been examined previously in micropipette-cannulated vessels or in endothelial monolayers in vitro. The primary objective of the current study was to determine whether acute changes in blood flow shear might influence measurements of L p in autoperfused, rather than cannulated, microvessels. In addition, a role for NO in shearmediated changes in L p was investigated. MATERIALS AND METHODSAnimal preparation. Animal procedures were approved by an Institutional Animal Care And Use Committee. Male Wistar rats ϳ2...

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Interaction of transmural pressure and shear stress in the transport of albumin across the rabbit aortic wall

Cited by 9 publications

References 25 publications

Effects of indoxyl sulfate on adherens junctions of endothelial cells and the underlying signaling mechanism

Effects of indoxyl sulfate on adherens junctions of endothelial cells and the underlying signaling mechanism

The pathogenesis of diabetic retinopathy: old concepts and new questions

Regulation of capillary hydraulic conductivity in response to an acute change in shear

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