Pulsatile flow enhances endothelium-derived nitric oxide release in the peripheral vasculature

Nakano, Toshihide; Tominaga, Ryuji; Nagano, Ichiro; Okabe, H; Yasui, Hirofumi

doi:10.1152/ajpheart.2000.278.4.h1098

Cited by 91 publications

(61 citation statements)

References 29 publications

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“…These findings are consistent with pG z activation of the Akt/PI3K pathway as a stimulus to eNOS activity, the latter via induced pulsations with circumferential stretch on the vascular endothelium. Our results also agree with in vitro endothelial cell culture findings of other investigators, who showed that pulsatile shear stress upregulates eNOS activity via the Akt/PI3K pathway (32,41,45,57).…”

Section: Discussionsupporting

confidence: 93%

“…However, there has been much less study of pulsatile shear stress alone in intact animals, with the exception of extracorporeal circulation, owing to the paucity of modalities to induce pulsatile shear stress in vivo (31,54). Nakano et al (41), in an extracorporeal model of pulsatile shear stress, found that eNOS activation is largely caused by tyrosine kinase-sensitive activation. In the present study, one such tyrosine kinase pathway, Akt/PI3K, was investigated by administration of WM that blocks this pathway.…”

Section: Discussionmentioning

confidence: 99%

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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: 93%

Section: Discussionmentioning

confidence: 99%

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

Uryash

Wu²,

Bassuk³

et al. 2009

Journal of Applied Physiology

View full text Add to dashboard Cite

show abstract

“…20 Endothelial-dependent vasodilation caused by elevated perfusion pulsatility has been confirmed in vascular beds other than the coronary arteries. For example, Nakano et al 21 reported that augmenting pulse perfusion in skeletal muscle triggers primary nitric oxide (NO)-dependent vasodilation. More recently, studies using external muscle compression to enhance central coronary blood flow revealed enhanced endothelial-dependent flow dilation in upper arm vascular beds exposed to the resulting higher perfusion pulsatility.…”

Section: Impact Of Blood Flow Pulsatilitymentioning

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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“…1992). The main cause of FMD has been shown as an endothelial release of nitric oxide (NO) (Nakano et al 2000) to regulate vascular d i a m e t e r, a n d r e fl e c t s t h e s e v e r i t y o f atherosclerosis (Celermajer 1997). FMD is used as a tool for quantifying endothelium-dependent vasodilatation, and impaired peripheral endothelial function may also be a marker of increased cardiovascular risk (Celermajer 1997).…”

Section: Cardiopulmonary Exercise Testingmentioning

confidence: 99%

Endothelial Flow-Mediated Dilatation and Exercise Capacity in Highly Trained Endurance Athletes

Kaşıkçıoğlu

Oflaz

Kaşıkçıoğlu

et al. 2005

Tohoku J. Exp. Med.

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Brachial artery ultrasound during reactive hyperemia is a noninvasive method of assessing peripheral endothelium-dependent vasodilatation. Aerobic exercise has the potential to improve local endothelial function. We sought to analyze the effects of regular aerobic training on brachial artery endothelial function in endurance athletes. We studied diameter and blood flow of the brachial artery in 32 endurance male athletes and 30 healthy male subjects. In the same subjects flow-mediated dilatation of the brachial artery was recorded by inducing an ischemia through a forearm arterial occluding cuff. Maximal oxygen consumption was significantly higher in the athletes group than in the controls (61.24 ± 5.43 vs 44.49 ± 2.68 ml/kg/min, p < 0.001). Flow-mediated dilatation of the brachial artery induced by forearm arterial occlusion in athletes was also higher than that of the control subjects (17.1 ± 2.3 vs 11.2 ± 1.7, p = 0.002). Furthermore, there was an association between flow-mediated dilatation and V O 2max (r = 0.69, p < 0.001). Baseline measurements of the diameter and the blood flow volume of the brachial artery were similar in both groups. During reactive hyperemia period, the percent of the changes of endothelial diameters and flow were significantly higher in athletes than in controls. Higher flowmediated dilatation levels in athletes reflect better vascular adaptation to habitual aerobic exercise.endothelium; athlete; exercise; nitric oxide

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Pulsatile flow enhances endothelium-derived nitric oxide release in the peripheral vasculature

Cited by 91 publications

References 29 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

Endothelial Flow-Mediated Dilatation and Exercise Capacity in Highly Trained Endurance Athletes

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