NADPH oxidase has a directional response to shear stress

Godbole, Anjali S.; Lu, Xiao; Guo, Xiaomei; Kassab, Ghassan S.

doi:10.1152/ajpheart.01251.2007

Cited by 59 publications

(40 citation statements)

References 61 publications

(98 reference statements)

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“…Six farm pigs weighing 28 Ϯ 5 kg were used in the study. The animal preparation was similar to that described previously (7,35). All animal experiments were performed in accordance with national and local ethical guidelines, including the Institute of Laboratory Animal Research Guide, Public Health Service policy, Animal Welfare Act, and IUPUI (Indiana University-Purdue University, Indianapolis) polices regarding the use of animals in research and received institutional approval.…”

Section: Methodsmentioning

confidence: 99%

Biaxial vasoactivity of porcine coronary artery

Huo¹,

Cheng²,

Zhao³

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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The passive mechanical properties of blood vessel mainly stem from the interaction of collagen and elastin fibers, but vessel constriction is attributed to smooth muscle cell (SMC) contraction. Although the passive properties of coronary arteries have been well characterized, the active biaxial stress-strain relationship is not known. Here, we carry out biaxial (inflation and axial extension) mechanical tests in right coronary arteries that provide the active coronary stress-strain relationship in circumferential and axial directions. Based on the measurements, a biaxial active strain energy function is proposed to quantify the constitutive stress-strain relationship in the physiological range of loading. The strain energy is expressed as a Gauss error function in the physiological pressure range. In K ϩ -induced vasoconstriction, the mean Ϯ SE values of outer diameters at transmural pressure of 80 mmHg were 3.41 Ϯ 0.17 and 3.28 Ϯ 0.24 mm at axial stretch ratios of 1.3 and 1.5, respectively, which were significantly smaller than those in Ca 2ϩ -free-induced vasodilated state (i.e., 4.01 Ϯ 0.16 and 3.75 Ϯ 0.20 mm, respectively). The mean Ϯ SE values of the inner and outer diameters in no-load state and the opening angles in zero-stress state were 1.69 Ϯ 0.04 mm and 2.25 Ϯ 0.08 mm and 126 Ϯ 22°, respectively. The active stresses have a maximal value at the passive pressure of 80 -100 mmHg and at the active pressure of 140 -160 mmHg. Moreover, a mechanical analysis shows a significant reduction of mean stress and strain (averaged through the vessel wall). These findings have important implications for understanding SMC mechanics.contraction; constitutive equation; stress-strain relation; vessel mechanics VASOACTIVITY OF LARGE EPICARDIAL coronary arteries is affected by cardiovascular diseases such as diabetes (14, 15), hypertension (14, 20), atherosclerosis (11), vasospasm (10, 32), and aneurysm (26), which are major risk factors for angina pectoris or myocardial infarction in patients. The constitutive passive and active stress-strain relationships can characterize the vasoactivity and are fundamental for understanding the mechanical behaviors of vascular smooth muscle cell (SMC) in health and disease (5). The strain energy function has been widely used to characterize the passive mechanical properties of blood vessels (5,8). For large epicardial coronary arteries, extensive mechanical measurements and analysis were carried out in the passive state (18,19,23,30,33,34).The active mechanical properties of coronary arteries are much known. To date, there are only uniaxial active constitutive length-tension relationships in the circumferential direction of coronary arteries (1, 2, 24, 31). Although some multi-axial active models have been proposed, those have been of theoretical forms not rooted in experimental measurements (25, 36). Clearly, there is a need for multi-axial active mechanical measurements and experimentally determined multi-dimensional active strain energy functions for coronary arteries.The objective ...

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Section: Methodsmentioning

confidence: 99%

Biaxial vasoactivity of porcine coronary artery

Huo¹,

Cheng²,

Zhao³

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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“…[13][14][15][16][17] Specifically, oscillatory shear reduces endothelial function and produces a pro-atherogenic gene expression pattern consisting of increased adhesion molecules, superoxide production, and monocyte recruitment. [14][15][16][17] Unfortunately, due to a paucity of literature in this area it is challenging to determine the impact that oscillatory shear plays in the maladaptive vascular structure reported in the lowerextremity arteries of SCI. Therefore, the purpose of this investigation was to elucidate hemodynamic differences in lower-extremity arteries of individuals with SCI compared to able-bodied individuals.…”

Section: Introductionmentioning

confidence: 99%

Altered resting hemodynamics in lower-extremity arteries of individuals with spinal cord injury

Bell

Chen

Bahls

et al. 2013

The Journal of Spinal Cord Medicine

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Objective: To investigate lower-extremity arterial hemodynamics in individuals with spinal cord injury (SCI). We hypothesized that oscillatory shear index would be altered and resting mean shear would be higher in the lowerextremity arteries of SCI. Research: Cross-sectional study of men and women with SCIs compared to able-bodied controls. Subjects: Subjects included 105 ages 18-72 years with American Spinal Injury Association (ASIA) Impairment Scale grades A, B, or C and injury duration at least 5 years. Subjects were matched for age and cardiovascular disease risk factors with 156 able-bodied controls. Methods: Diameter and blood velocity were determined with subject at rest via ultrasound in superficial femoral, popliteal, brachial, and carotid arteries. Mean shear, antegrade shear, retrograde shear, and oscillatory shear index were calculated. Results: Oscillatory shear index was lower in SCI compared to controls for superficial femoral (0.16 ± 0.10 vs. 0.26 ± 0.06, P < 0.01) and popliteal arteries (0.20 ± 0.11 vs. 0.26 ± 0.05, P < 0.01). Mean shear rate was higher in SCI compared to controls for superficial femoral (43.54 ± 28.0 vs. 20.48 ± 13.1/second, P < 0.01) and popliteal arteries (30.43 ± 28.1 vs. 11.68 ± 9.5/second, P < 0.01). Conclusions: The altered resting hemodynamics in SCI are consistent with an atheroprotective hemodynamic environment.

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“…In the same study, PMA stimulated ROS production in cultured endothelial cells, but not in cultured smooth muscle cells. We have previously shown (15) in an in vitro blood vessel preparation that the major source of ROS/O 2 ·Ϫ during complete reversed flow is the NADPH oxidase.…”

Section: Discussionmentioning

confidence: 99%

“…Although the cause of endothelial cell dysfunction due to change in WSS may be complex, increased evidence suggests that excessive production of reactive oxygen species (ROS) may play an important role in this process. We have previously shown that NADPH oxidase has a directional response to shear stress (15).…”

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confidence: 99%

Endothelial actin depolymerization mediates NADPH oxidase-superoxide production during flow reversal

Choy

Yang

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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Slow moving blood flow and changes in flow direction, e.g., negative wall shear stress, can cause increased superoxide (O2 ·Ϫ ) production in vascular endothelial cells. The mechanism by which shear stress increases O2·Ϫ production, however, is not well established. We tested the hypothesis that actin depolymerization, which occurs during flow reversal, mediates O2 ·Ϫ production in vascular endothelial cells via NADPH oxidase, and more specifically, the subunit p47 phox . Using a swine model, we created complete blood flow reversal in one carotid artery, while the contralateral vessel maintained forward blood flow as control. We measured actin depolymerization, NADPH oxidase activity, and reactive oxygen species (ROS) production in the presence of various inhibitors. Flow reversal was found to induce actin depolymerization and a 3.9 Ϯ 1.0-fold increase in ROS production as compared with forward flow. NADPH oxidase activity was 1.4 Ϯ 0.2 times higher in vessel segments subjected to reversed blood flow when measured by a direct enzyme assay. The NADPH oxidase subunits gp91 phox (Nox2) and p47 phox content in the vessels remained unchanged after 4 h of flow reversal. In contrast, p47 phox phosphorylation was increased in vessels with reversed flow. The response caused by reversed flow was reduced by in vivo treatment with jasplakinolide, an actin stabilizer (only a 1.7 Ϯ 0.3-fold increase). Apocynin (an antioxidant) prevented reversed flow-induced ROS production when the animals were treated in vivo. Cytochalasin D mimicked actin depolymerization in vitro and caused a 5.2 Ϯ 3.0-fold increase in ROS production. These findings suggest that actin filaments play an important role in negative shear stress-induced ROS production by potentiating NADPH oxidase activity, and more specifically, the p47 phox subunit in vascular endothelium.endothelial cells

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NADPH oxidase has a directional response to shear stress

Cited by 59 publications

References 61 publications

Biaxial vasoactivity of porcine coronary artery

Biaxial vasoactivity of porcine coronary artery

Altered resting hemodynamics in lower-extremity arteries of individuals with spinal cord injury

Endothelial actin depolymerization mediates NADPH oxidase-superoxide production during flow reversal

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