Endothelial nitric oxide production during in vitro simulation of external limb compression

Dai, Guohao; Tsukurov, Olga; Chen, Michael; Gertler, Jonathan P.; Kamm, Roger D.

doi:10.1152/ajpheart.00288.2001

Cited by 33 publications

(27 citation statements)

References 40 publications

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“…They found optimum frequencies for vasodilatation to be between 240 and 360 cpm, with frequencies below and above yielding lower percent vasodilation (25). Our findings are also consistent with findings from the enhanced external counterpulsation data, wherein timed diastolic pulsations have been shown to improve diastolic endothelial function and NO production (2, 8,14,17,24,35). Unlike enhanced external counterpulsation, pG z is not timed to systole or diastole, but its effects on eNOS production and other beneficial endothelial-derived mediators have been established (4,36,39,48).…”

Section: Discussionsupporting

confidence: 88%

Low-amplitude pulses to the circulation through periodic acceleration induces endothelial-dependent vasodilatation

Uryash

Wu²,

Bassuk³

et al. 2009

Journal of Applied Physiology

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Uryash A, Wu H, Bassuk J, Kurlansky P, Sackner MA, Adams JA. Low-amplitude pulses to the circulation through periodic acceleration induces endothelial-dependent vasodilatation. J Appl Physiol 106: 1840 -1847, 2009. First published March 26, 2009 doi:10.1152/japplphysiol.91612.2008.-Low-amplitude pulses to the vasculature increase pulsatile shear stress to the endothelium. This activates endothelial nitric oxide (NO) synthase (eNOS) to promote NO release and endothelial-dependent vasodilatation. Descent of the dicrotic notch on the arterial pulse waveform and a-to-b ratio (a/b; where a is the height of the pulse amplitude and b is the height of the dicrotic notch above the end-diastolic level) reflects vasodilator (increased a/b) and vasoconstrictor effects (decreased a/b) due to NO level change. Periodic acceleration (pG z) (motion of the supine body head to foot on a platform) provides systemic additional pulsatile shear stress. The purpose of this study was to determine whether or not pG z applied to rats produced endothelial-dependent vasodilatation and increased NO production, and whether the latter was regulated by the Akt/phosphatidylinositol 3-kinase (PI3K) pathway. Male rats were anesthetized and instrumented, and pG z was applied. Sodium nitroprusside, N G -nitro-L-arginine methyl ester (L-NAME), and wortmannin (WM; to block Akt/PI3K pathway) were administered to compare changes in a/b and mean aortic pressure. Descent of the dicrotic notch occurred within 2 s of initiating pG z. Dose-dependent increase of a/b and decrease of mean aortic pressure took place with SNP. L-NAME produced a dose-dependent rise in mean aortic pressure and decrease of a/b, which was blunted with pG z. In the presence of WM, pGz did not decrease aortic pressure or increase a/b. WM also abolished the pG z blunting effect on blood pressure and a/b of L-NAME-treated animals. eNOS expression was increased in aortic tissue after pG z. This study indicates that addition of low-amplitude pulses to circulation through pG z produces endothelial-dependent vasodilatation due to increased NO in rats, which is mediated via activation of eNOS, in part, by the Akt/PI3K pathway. vascular resistance; N G -nitro-L-arginine methyl ester, wortmannin; nitric oxide ADDED LOW-AMPLITUDE PULSES to the vasculature were generated with periodic acceleration (pG z ). pG z is produced by a motorized platform that repetitively moves the horizontally oriented body sinusoidally in a head to foot direction. Inertia of fluid as the body accelerates and decelerates adds a small-amplitude pulse to the circulation that is superimposed on the natural pulse, increasing pulsatile shear stress to the endothelium (3, 6, 7). In large-animal models, increased pulsatile shear stress activates endothelial nitric oxide (NO) synthase (eNOS) to release NO into the circulation, which, in turn, induces endothelial-dependent pulmonary and systemic vasodilatation, as well as increasing organ blood flows (3,5,6). pG z applied to anesthetized swine increases serum nitrite, which is ...

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Section: Discussionsupporting

confidence: 88%

Low-amplitude pulses to the circulation through periodic acceleration induces endothelial-dependent vasodilatation

Uryash

Wu²,

Bassuk³

et al. 2009

Journal of Applied Physiology

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“…This is further supported by data showing enhanced NO release from endothelial cells grown in distensible tubes exposed to pulsatile flow from external compression. 34 …”

Section: Role Of Wall Distensibilitymentioning

confidence: 99%

Ventricular Arterial Stiffening

2005

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Abstract-Vascular stiffening of the large arteries is a common feature of aging and is exacerbated by many common disorders such as hypertension, diabetes, and renal disease. This change influences the phasic mechanical stresses imposed on the blood vessels that in turn is important to regulating smooth muscle tone, endothelial function, and vascular health. In addition, the heart typically adapts to confront higher and later systolic loads by both hypertrophy and ventricular systolic stiffening. This creates altered coupling between heart and vessel that importantly affects cardiovascular reserve function. In this overview, I discuss the notion of a coupling disease in which stiffness of both heart and arteries interact to limit performance and generate clinical symptoms. This involves changes in the mechanical interaction of both systems, changes in signaling within the arteries themselves, and alterations in coronary flow regulation. Lastly, I briefly review recent development in de-stiffening strategies that may pave the way to treat this syndrome and its clinical manifestations.

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“…Walshe et al [25] described a pulsatile flow system in which a co-culture of endothelial and smooth muscle cells showed an increase in both NO and ET-1 production with flow. Dai et al [26] found that endothelial cells up-regulated NO synthesis with the flow in a venous flow simulator, while there were no differences in ET-1 production. Using a combined pressurized flow and a cyclic strain, Tsukurov et al [27] reported that ET-1 production was down-regulated after 48 h, but not after 24 h, whereas the results for NO production were not clear.…”

Section: Introductionmentioning

confidence: 99%

Hydrostatic pressure and shear stress affect endothelin‐1 and nitric oxide release by endothelial cells in bioreactors

Vozzi

Bianchi

Ahluwalia

et al. 2013

Biotechnology Journal

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Abundant experimental evidence demonstrates that endothelial cells are sensitive to flow; however, the effect of fluid pressure or pressure gradients that are used to drive viscous flow is not well understood. There are two principal physical forces exerted on the blood vessel wall by the passage of intra-luminal blood: pressure and shear. To analyze the effects of pressure and shear independently, these two stresses were applied to cultured cells in two different types of bioreactors: a pressure-controlled bioreactor and a laminar flow bioreactor, in which controlled levels of pressure or shear stress, respectively, can be generated. Using these bioreactor systems, endothelin-1 (ET-1) and nitric oxide (NO) release from human umbilical vein endothelial cells were measured under various shear stress and pressure conditions. Compared to the controls, a decrease of ET-1 production by the cells cultured in both bioreactors was observed, whereas NO synthesis was up-regulated in cells under shear stress, but was not modulated by hydrostatic pressure. These results show that the two hemodynamic forces acting on blood vessels affect endothelial cell function in different ways, and that both should be considered when planning in vitro experiments in the presence of flow. Understanding the individual and synergic effects of the two forces could provide important insights into physiological and pathological processes involved in vascular remodeling and adaptation.

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Endothelial nitric oxide production during in vitro simulation of external limb compression

Cited by 33 publications

References 40 publications

Low-amplitude pulses to the circulation through periodic acceleration induces endothelial-dependent vasodilatation

Low-amplitude pulses to the circulation through periodic acceleration induces endothelial-dependent vasodilatation

Ventricular Arterial Stiffening

Hydrostatic pressure and shear stress affect endothelin‐1 and nitric oxide release by endothelial cells in bioreactors

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