Pulsatile Stretch and Shear Stress: Physical Stimuli Determining the Production of Endothelium-Derived Relaxing Factors

Busse, Rudi; Fleming, Ingrid

doi:10.1159/000025568

Cited by 227 publications

(160 citation statements)

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“…Molecular biological studies have shown that a low average level, large gradients, and high oscillation of wall shear stress (WSS) contribute to atherosclerosis [1][2][3]. Therefore, the triggering of atherosclerosis by WSS is widely acknowledged.…”

Section: Introductionmentioning

confidence: 99%

Spatial Distribution of Wall Shear Stress in Common Carotid Artery by Color Doppler Flow Imaging

et al. 2012

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The purpose of this study is to provide a novel approach for measuring the spatial distribution of wall shear stress (WSS) in common carotid artery in vivo. WSS distributions were determined by digital image processing from color Doppler flow imaging (CDFI) in 50 healthy volunteers. In order to evaluate the feasibility of the spatial distribution, the mean values of WSS distribution were compared to the results of conventional WSS calculating method (Hagen-Poiseuille formula). In our study, the mean value of WSS distribution from 50 healthy volunteers was (6.91 ± 1.20) dyne/cm 2 , while it was (7.13 ± 1.24) dyne/cm 2 by Hagen-Poiseuille approach. The difference was not statistically significant (t 0−0.864, p 00.604). Hence, the feasibility of the spatial distribution of WSS was proved. Moreover, this novel approach could provide three-dimensional distribution of shear stress and fusion image of shear stress with ultrasonic image for each volunteer, which made WSS "visible". In conclusion, the spatial distribution of WSS could be used for WSS calculation in vivo. Moreover, it could provide more detailed values of WSS distribution than those of Hagen-Poiseuille formula.

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Section: Introductionmentioning

confidence: 99%

Spatial Distribution of Wall Shear Stress in Common Carotid Artery by Color Doppler Flow Imaging

et al. 2012

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“…It is suggested that increased vascular wall shear stress associated with acute bouts of aerobic exercise may represent the main stimulus for vascular adaptations induced by chronic aerobic exercise (3,39,41). Accordingly, chronic aerobic exercise of moderate intensity is considered to have beneficial effects in cardiovascular diseases involving endothelial dysfunction (11,14,16,17).…”

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confidence: 99%

“…In this context, endothelium-dependent vasodilation induced by acetylcholine (ACh), which is known to produce NO-dependent vascular relaxation, has been used to characterize endothelium function in different physiological and pathophysiological conditions both in animal and human studies (7). Vascular reactivity can also be modulated by an endothelium-derived hyperpolarizing factor (EDHF), which probably acts through the activation of Ca 2ϩ -sensitive K ϩ channels (3). EDHF seems to be essentially involved in the local regulation of blood flow in small resistance vessels (10,37), with the exception of the coronary and renal vascular beds where it also contributes to the modulation of vascular reactivity in conduit arteries (3).…”

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confidence: 99%

“…Vascular reactivity can also be modulated by an endothelium-derived hyperpolarizing factor (EDHF), which probably acts through the activation of Ca 2ϩ -sensitive K ϩ channels (3). EDHF seems to be essentially involved in the local regulation of blood flow in small resistance vessels (10,37), with the exception of the coronary and renal vascular beds where it also contributes to the modulation of vascular reactivity in conduit arteries (3). Endothelium dysfunction, which can be evidenced by an impairment in endothelium-dependent relaxation, plays a pivotal role in the pathogenesis of cardiovascular diseases, such as arterial hypertension and coronary heart disease (54), as well as in diabetic angiopathy (13).…”

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confidence: 99%

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Effects of exercise training on the vascular reactivity of the whole kidney circulation in rabbits

Moraes¹,

Gioseffi²,

Nóbrega³

et al. 2004

Journal of Applied Physiology

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is known to improve vasodilating mechanisms mediated by endothelium-dependent relaxing factors in the cardiac and skeletal muscle vascular beds. However, the effects of exercise training on visceral vascular reactivity, including the renal circulation, are still unclear. We used the experimental model of the isolated perfused rabbit kidney, which involves both the renal macro-and microcirculation, to test the hypothesis that exercise training improves vasodilator mechanisms in the entire renal circulation. New Zealand White rabbits were pen confined (Sed; n ϭ 24) or treadmill trained (0% grade) for 5 days/wk at a speed of 18 m/min during 60 min over a 12-wk period (ExT; n ϭ 24). Kidneys isolated from Sed and ExT rabbits were continuously perfused in a nonrecirculating system under conditions of constant flow and precontracted with norepinephrine (NE). We assessed the effects of exercise training on renal vascular reactivity using endothelial-dependent [acetylcholine (ACh) and bradykinin (BK)] and -independent [sodium nitroprusside (SNP)] vasodilators. ACh induced marked and dose-related vasodilator responses in kidneys from Sed rabbits, the reduction in perfusion pressure reaching 41 Ϯ 8% (n ϭ 6; P Ͻ 0.05). In the kidneys from ExT rabbits, vasodilation induced by ACh was significantly enhanced to 54 Ϯ 6% (n ϭ 6; P Ͻ 0.05). In contrast, BK-induced renal vasodilation was not enhanced by training [19 Ϯ 8 and 13 Ϯ 4% reduction in perfusion pressure for Sed and ExT rabbits, respectively (n ϭ 6; P Ͼ 0.05)]. Continuous perfusion of isolated kidneys from ExT animals with N -nitro-L-arginine methyl ester (L-NAME; 300 M), an inhibitor of nitric oxide (NO) biosynthesis, completely blunted the additional vasodilation elicited by ACh [reduction in perfusion pressure of 54 Ϯ 6 and 38 Ϯ 5% for ExT and L-NAME ϩ ExT, respectively (n ϭ 6; P Ͻ 0.05)]. On the other hand, L-NAME infusion did not affect ACh-induced vasodilation in Sed animals. Exercise training also increased renal vasodilation induced by SNP [36 Ϯ 7 and 45 Ϯ 10% reduction in perfusion pressure for Sed and ExT rabbits, respectively (n ϭ 6; P Ͻ 0.05)]. It is concluded that exercise training alters the rabbit kidney vascular reactivity, enhancing endothelium-dependent and -independent renal vasodilation. This effect seems to be related not only to an increased bioavailability of NO but also to the enhanced responsiveness of the renal vascular smooth muscle to NO. chronic exercise; endothelial dysfunction; isolated perfused rabbit kidney IT IS WELL KNOWN THAT THE endothelium plays a role of paramount importance in the regulation of the vasomotor tone (for review, see Ref. 26). The endothelial cells synthesize and release several relaxing and contracting diffusible substances that interact with the underlying vascular smooth muscle, thus contributing to the continuous modulation of vascular reactivity (26). The best-characterized endothelium-derived relaxing factors are nitric oxide (NO) and prostacyclin (PGI 2 ), which can be released by physical (shear stress by the fl...

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“…Recently, a correlation with changes in functional residual capacity (FRC) has led to the suggestion that mechanical stretching of lung tissue might be one underlying mechanism modulating lower airway NO formation (Str omberg et al 1997). Similar stretchresponsive mechanisms influencing NO release have been established in both striated muscle and endothelial cells (Awolesi et al 1995;Tidball et al 1998;Busse & Fleming, 1998). The amount of NO released from endothelial cells in response to a mechanical stimulus is determined by the timing and amplitude of the physical forces applied (Hutcheson & Griffith, 1991).…”

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confidence: 99%

Exhaled Nitric Oxide Increases During High Frequency Oscillatory Ventilation in Rabbits

Artlich¹,

Adding²,

Agvald³

et al. 1999

Exp. Physiol.

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summaryThis study compared the effects of high frequency oscillatory ventilation (HFOV) and intermittent mandatory ventilation (IMV) on the homeostasis of nitric oxide (NO) in the lower respiratory tract of healthy rabbits. The mechanisms underlying a putative stretch response of NO formation in the airways were further elucidated. Male New Zealand White rabbits were anaesthetized, tracheotomized and ventilated with IMV or HFOV in random order. Total NO excretion increased from 9·6 ± 0·8 nl min¢ (mean ± s.e.m.) during IMV to 22·6 ± 2·7 nl min¢ during HFOV (P < 0·001). This increase was not explained by changes of functional residual capacity (ÄFRC). A similar increase in NO excretion during HFOV was seen in isolated buffer-perfused lungs under constant circulatory conditions (P < 0·05, n = 4). Intratracheal mean COµ and NO concentrations, measured at 2·5, 5, 7·5 and 10 cm below tracheostomy, increased significantly with increasing distance into the lung during both IMV and HFOV (P < 0·001 for each comparison). At every intratracheal location of the sampling catheter, particularly low in the airways, both COµ and NO concentrations were significantly higher during HFOV than during IMV (P < 0·01 for each comparison). We conclude that HFOV increases pulmonary NO production in healthy rabbits. Increased stretch activation of the respiratory system during HFOV is suggested as a possible underlying mechanism. The increase in mean airway NO concentrations may have biological effects in the respiratory tract. Whether it can account for some of the benefits of HFOV treatment needs to be considered. introduction NO, which is continuously produced within the lower respiratory tract (Gustafsson et al. 1991;Persson et al. 1993), can be detected in the exhaled gas of most mammalian species, offering a unique possibility to study features of NO metabolism non-invasively (Gustafsson, 1997). However, the anatomic site and main cell type producing those NO molecules detected in exhaled gas is still a matter of debate (Gustafsson, 1997). Thus the extent to which the various biological functions of NO are reflected in the concentration of NO in exhaled gas merits further study. Moreover, factors influencing the amount of NO detected in exhaled gas are only beginning to evolve. We have recently shown in rabbits and guinea-pigs that lower airway NO formation is suppressed by high airway concentrations of COµ Str omberg et al. 1997;Adding et al. 1999). This rapid effect is also present in isolated buffer-perfused rabbit lungs and cannot be explained by either altered sympathetic outflow or changes of extracellular pH (Adding et al. 1999). Another mechanism to increase lower airway NO formation is revealed during increases of positive end-expiratory pressure (PEEP)

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Pulsatile Stretch and Shear Stress: Physical Stimuli Determining the Production of Endothelium-Derived Relaxing Factors

Cited by 227 publications

References 103 publications

Spatial Distribution of Wall Shear Stress in Common Carotid Artery by Color Doppler Flow Imaging

Spatial Distribution of Wall Shear Stress in Common Carotid Artery by Color Doppler Flow Imaging

Effects of exercise training on the vascular reactivity of the whole kidney circulation in rabbits

Exhaled Nitric Oxide Increases During High Frequency Oscillatory Ventilation in Rabbits

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