Flow Induced Vasodilation in Porcine Carotid Arteries

2012 ◽  
Author(s):  
Renate W. Boekhoven ◽  
Tatjana Maas ◽  
Marcel C. M. Rutten ◽  
Frans N. van de Vosse
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Shear Stress ◽  
Carotid Arteries ◽  
Physiological Flow ◽  
Vasoactive Substances ◽  
Cardiovascular Pathologies

Endothelial cells play an important role in the autoregulation of the vascular diameter for maintaining physiological flow and shear stress. An increase in blood flow causes an increase in shear stress, which is sensed by the endothelial cells, resulting in the release of vasoactive substances. An impaired endothelial mediated vasomotive response seems reflective for several cardiovascular pathologies, such as failure of atherosclerosis and arterio-venous fistulas (AVF).

Microvascular dilation in response to occlusion: a coordinating role for conducted vasomotor responses

2000 ◽  
Vol 279 (1) ◽  
pp. H279-H284 ◽  
Author(s):  
Kim A. Dora ◽  
David N. Damon ◽  
Brian R. Duling
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Shear Stress ◽  
Smooth Muscle ◽  
Third Order ◽  
Vasomotor Responses ◽  
Vasodilatory Response ◽  
Flow Through ◽  
Stress Dependent ◽  
Dependent Mechanism

In rat cremasteric microcirculation, mechanical occlusion of one branch of an arteriolar bifurcation causes an increase in flow and vasodilation of the unoccluded daughter branch. This dilation has been attributed to the operation of a shear stress-dependent mechanism in the microcirculation. Instead of or in addition to this, we hypothesized that the dilation observed during occlusion is the result of a conducted signal originating distal to the occlusion. To test this hypothesis, we blocked the ascending spread of conducted vasomotor responses by damaging the smooth muscle and endothelial cells in a 200-μm segment of second- or third-order arterioles. We found that a conduction blockade eliminated or diminished the occlusion-associated increase in flow through the unoccluded branch and abolished or strongly attenuated the vasodilatory response in both vessels at the branch. We also noted that vasodilations induced by ACh (10−4 M, 0.6 s) spread to, but not beyond, the area of damage. Taken together, these data provide strong evidence that conducted vasomotor responses have an important role in coordinating blood flow in response to an arteriolar occlusion.

Shear stress and 17β-estradiol modulate cerebral microvascular endothelial Na-K-Cl cotransporter and Na/H exchanger protein levels

2008 ◽  
Vol 294 (1) ◽  
pp. C363-C371 ◽  
Author(s):  
Elaine Chang ◽  
Martha E. O'Donnell ◽  
Abdul I. Barakat
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Shear Stress ◽  
Ischemic Stroke ◽  
Edema Formation ◽  
Protein Levels ◽  
Prominent Component ◽  
17Β Estradiol ◽  
Microvascular Endothelial ◽  
Brain Edema Formation

Ion transporters of blood-brain barrier (BBB) endothelial cells play an important role in regulating the movement of ions between the blood and brain. During ischemic stroke, reduction in cerebral blood flow is accompanied by transport of Na and Cl from the blood into the brain, with consequent brain edema formation. We have shown previously that a BBB Na-K-Cl cotransporter (NKCC) participates in ischemia-induced brain Na and water uptake and that a BBB Na/H exchanger (NHE) may also participate. While the abrupt reduction of blood flow is a prominent component of ischemia, the effects of flow on BBB NKCC and NHE are not known. In the present study, we examined the effects of changes in shear stress on NKCC and NHE protein levels in cerebral microvascular endothelial cells (CMECs). We have shown previously that estradiol attenuates both ischemia-induced cerebral edema and CMEC NKCC activity. Thus, in the present study, we also examined the effects of estradiol on NKCC and NHE protein levels in CMECs. Exposing CMECs to steady shear stress (19 dyn/cm2) increased the abundance of both NKCC and NHE. Estradiol abolished the shear stress-induced increase in NHE but not NKCC. Abrupt reduction of shear stress did not alter NKCC or NHE abundance in the absence of estradiol, but it decreased NKCC abundance in estradiol-treated cells. Our results indicate that changes in shear stress modulate BBB NKCC and NHE protein levels. They also support the hypothesis that estradiol attenuates edema formation in ischemic stroke in part by reducing the abundance of BBB NKCC protein.

scholarly journals Shear stress and aneurysms: a review

2019 ◽  
Vol 47 (1) ◽  
pp. E2 ◽  
Author(s):  
Brittany Staarmann ◽  
Matthew Smith ◽  
Charles J. Prestigiacomo
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Shear Stress ◽  
Smooth Muscle ◽  
Wall Shear Stress ◽  
Smooth Muscle Cells ◽  
Frictional Force ◽  
Vessel Wall ◽  
Risk Of Rupture ◽  
Aneurysm Growth

Wall shear stress, the frictional force of blood flow tangential to an artery lumen, has been demonstrated in multiple studies to influence aneurysm formation and risk of rupture. In this article, the authors review the ways in which shear stress may influence aneurysm growth and rupture through changes in the vessel wall endothelial cells, smooth-muscle cells, and surrounding adventitia, and they discuss shear stress–induced pathways through which these changes occur.

scholarly journals Heg1 and Ccm1/2 proteins control endocardial mechanosensitivity during zebrafish valvulogenesis

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Stefan Donat ◽  
Marta Lourenço ◽  
Alessio Paolini ◽  
Cécile Otten ◽  
Marc Renz ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Shear Stress ◽  
Fluid Shear Stress ◽  
Cavernous Malformation ◽  
Cardiac Valve ◽  
Valve Leaflet ◽  
Fluid Shear ◽  
Binding Partner ◽  
Different Levels

Endothelial cells respond to different levels of fluid shear stress through adaptations of their mechanosensitivity. Currently, we lack a good understanding of how this contributes to sculpting of the cardiovascular system. Cerebral cavernous malformation (CCM) is an inherited vascular disease that occurs when a second somatic mutation causes a loss of CCM1/KRIT1, CCM2, or CCM3 proteins. Here, we demonstrate that zebrafish Krit1 regulates the formation of cardiac valves. Expression of heg1, which encodes a binding partner of Krit1, is positively regulated by blood-flow. In turn, Heg1 stabilizes levels of Krit1 protein, and both Heg1 and Krit1 dampen expression levels of klf2a, a major mechanosensitive gene. Conversely, loss of Krit1 results in increased expression of klf2a and notch1b throughout the endocardium and prevents cardiac valve leaflet formation. Hence, the correct balance of blood-flow-dependent induction and Krit1 protein-mediated repression of klf2a and notch1b ultimately shapes cardiac valve leaflet morphology.

scholarly journals Shear stress, arterial identity and atherosclerosis

2016 ◽  
Vol 115 (03) ◽  
pp. 467-473 ◽  
Author(s):  
Elizabeth A. Jones ◽  
Stephanie Lehoux
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Shear Stress ◽  
Inflammatory Diseases ◽  
Branch Points ◽  
Laminar Shear Stress ◽  
Specific Expression ◽  
Temporal Cues ◽  
Expression Of Genes ◽  
Atherosclerosis Risk Factors

SummaryIn the developing embryo, the vasculature first takes the form of a web-like network called the vascular plexus. Arterial and venous differentiation is subsequently guided by the specific expression of genes in the endothelial cells that provide spatial and temporal cues for development. Notch1/4, Notch ligand delta-like 4 (Dll4), and Notch downstream effectors are typically expressed in arterial cells along with EphrinB2, whereas chicken ovalbumin upstream promoter transcription factor II (COUP-TFII) and EphB4 characterise vein endothelial cells. Haemodynamic forces (blood pressure and blood flow) also contribute importantly to vascular remodelling. Early arteriovenous differentiation and local blood flow may hold the key to future inflammatory diseases. Indeed, despite the fact that atherosclerosis risk factors such as smoking, hypertension, hypercholesterolaemia, and diabetes all induce endothelial cell dysfunction throughout the vasculature, plaques develop only in arteries, and they localise essentially in vessel branch points, curvatures and bifurcations, where blood flow (and consequently shear stress) is low or oscillatory. Arterial segments exposed to high blood flow (and high laminar shear stress) tend to remain plaque-free. These observations have led many to investigate what particular properties of arterial or venous endothelial cells confer susceptibility or protection from plaque formation, and how that might interact with a particular shear stress environment.

scholarly journals Mechanosensitive molecular interactions in atherogenic regions of the arteries: development of atherosclerosis

2021 ◽  
Vol 25 (5) ◽  
pp. 552-561
Author(s):  
E. L. Mishchenko ◽  
A. M. Mishchenko ◽  
V. A. Ivanisenko
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Shear Stress ◽  
Cell Adhesion ◽  
Wall Shear Stress ◽  
Signaling Pathways ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Mechanical Stimulus ◽  
Wall Shear

A terrible disease of the cardiovascular system, atherosclerosis, develops in the areas of bends and branches of arteries, where the direction and modulus of the blood flow velocity vector change, and consequently so does the mechanical effect on endothelial cells in contact with the blood flow. The review focuses on topical research studies on the development of atherosclerosis – mechanobiochemical events that transform the proatherogenic mechanical stimulus of blood flow – low and low/oscillatory arterial wall shear stress in the chains of biochemical reactions in endothelial cells, leading to the expression of specific proteins that cause the progression of the pathological process. The stages of atherogenesis, systemic risk factors for atherogenesis and its important hemodynamic factor, low and low/oscillatory wall shear stress exerted by blood flow on the endothelial cells lining the arterial walls, have been described. The interactions of cell adhesion molecules responsible for the development of atherosclerosis under low and low/oscillating shear stress conditions have been demonstrated. The activation of the regulator of the expression of cell adhesion molecules, the transcription factor NF­κB, and the factors regulating its activation under these conditions have been described. Mechanosensitive signaling pathways leading to the expression of NF­κB in endothelial cells have been described. Studies of the mechanobiochemical signaling pathways and interactions involved in the progression of atherosclerosis provide valuable information for the development of approaches that delay or block the development of this disease.

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