Reactive oxygen species alter contractile properties of pulmonary arterial smooth muscle

Rhoades, Rodney A.; Packer, C. Subah; Roepke, D.A.; Jin, Najia; Meiss, Richard A.

doi:10.1139/y90-241

Cited by 103 publications

(59 citation statements)

References 20 publications

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“…Another study showed that H 2 O 2 at low concentration caused vasorelaxation, but, at millimolar concentration, it activated vasoconstriction in hypoxia-contracted guinea pig pulmonary arteries (1). In contrast, H 2 O 2 -induced pulmonary vasoconstriction has been reported in many other studies in the absence of agonist-induced preconstriction (26,46,50,56). Depending on the preparations, H 2 O 2 -induced pulmonary vasoconstriction has been attributed to the activation of different signaling pathways, including cyclooxygenase, lipoxygenase, calmodulin, protein kinase C, phospholipase C, serine esterase, and tyrosine kinase.…”

Section: Methodsmentioning

confidence: 89%

Hydrogen peroxide-induced Ca²⁺mobilization in pulmonary arterial smooth muscle cells

Lin

Yang

Cao

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

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March 16, 2007; doi:10.1152/ajplung.00323.2006.-Reactive oxygen species (ROS) generated from NADPH oxidases and mitochondria have been implicated as key messengers for pulmonary vasoconstriction and vascular remodeling induced by agonists and hypoxia. Since Ca 2ϩ mobilization is essential for vasoconstriction and cell proliferation, we sought to characterize the Ca 2ϩ response and to delineate the Ca 2ϩ pathways activated by hydrogen peroxide (H2O2) in rat intralobar pulmonary arterial smooth muscle cells (PASMCs). Exogenous application of 10 M to 1 mM H 2O2 elicited concentration-dependent increase in intracellular Ca 2ϩ concentration in PASMCs, with an initial rise followed by a plateau or slow secondary increase. The initial phase was related to intracellular release. It was attenuated by the inositol trisphosphate (IP 3) receptor antagonist 2-aminoethyl diphenylborate, ryanodine, or thapsigargin, but was unaffected by the removal of Ca 2ϩ in external solution. The secondary phase was dependent on extracellular Ca 2ϩ influx. It was unaffected by the voltage-gated Ca 2ϩ channel blocker nifedipine or the nonselective cation channel blockers SKF-96365 and La 3ϩ , but inhibited concentration dependently by millimolar Ni 2ϩ , and potentiated by the Na ϩ /Ca 2ϩ exchange inhibitor KB-R 7943. H2O2 did not alter the rate of Mn 2ϩ quenching of fura 2, suggesting store-and receptor-operated Ca 2ϩ channels were not involved. By contrast, H2O2 elicited a sustained inward current carried by Na ϩ at Ϫ70 mV, and the current was inhibited by Ni 2ϩ . These results suggest that H2O2 mobilizes intracellular Ca 2ϩ through multiple pathways, including the IP3-and ryanodine receptor-gated Ca 2ϩ stores, and Ni 2ϩ -sensitive cation channels. Activation of these Ca 2ϩ pathways may play important roles in ROS signaling in PASMCs.nonselective cation channels; sodium-calcium exchange; ryanodine receptor; inositol trisphosphate receptor; pulmonary arteries REACTIVE OXYGEN SPECIES (ROS) derived from diverse cellular sources, including NADPH oxidase, mitochondrial electron transport chain (ETC), xanthine oxidase, cytochrome P-450, cyclooxygenase, and nitric oxide synthase, are known to play important roles in the regulation of pulmonary and systemic circulation (15). It has been established that vasoconstrictors/ mitogens, such as angiotensin II, serotonin, endothelin-1, platelet-derived growth factor, and tumor necrosis factor-␣, stimulate the production of superoxide and hydrogen peroxide (H 2 O 2 ) to enhance vasoconstriction and activate redox-sensitive gene transcription to promote proliferation, hypertrophy, migration, and survival of vascular smooth muscle cell (14,34,36,58). Recent studies showed that ROS overproduction is associated with pulmonary remodeling and alterations in vascular reactivity observed in chronic hypoxia, and targeted deletion of gp91 phox subunit prevented these changes in knockout mice, suggesting that ROS generated from NADPH oxidase contribute significantly to the pathogenesis of hypoxic pulmonary hypertens...

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Section: Methodsmentioning

confidence: 89%

Hydrogen peroxide-induced Ca²⁺mobilization in pulmonary arterial smooth muscle cells

Lin

Yang

Cao

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…For example, H 2 O 2 elicits vasoconstriction in the canine basilar artery (20) and rat aorta (51) but produces dilation in the rabbit aorta (52). A biphasic response consisting of a transient contraction, followed by relaxation was observed in the rat pulmonary artery (33). The contradictory results, either constriction (37) or dilation (5) of rabbit intrapulmonary arteries, were also reported.…”

Section: Discussionmentioning

confidence: 99%

Hydrogen peroxide induces endothelium-dependent and -independent coronary arteriolar dilation: role of cyclooxygenase and potassium channels

Thengchaisri

2003

American Journal of Physiology-Heart and Circulatory Physiology

140

122

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Thengchaisri, Naris, and Lih Kuo. Hydrogen peroxide induces endothelium-dependent and -independent coronary arteriolar dilation: role of cyclooxygenase and potassium channels. Am J Physiol Heart Circ Physiol 285: H2255-H2263, 2003;; 10.1152/ajpheart.00487.2003.-Hydrogen peroxide, a relatively stable reactive oxygen species, is known to elicit vasodilation, but its underlying mechanism remains elusive. Here, we examined the role of endothelial nitric oxide (NO), prostaglandin, cytochrome P-450-derived metabolites, and smooth muscle potassium channels in coronary arteriolar dilation to abluminal H 2O2. Pig subepicardial coronary arterioles (50-100 m) were isolated and pressurized without flow for in vitro study. Arterioles developed basal tone and dilated dose dependently to H 2O2 (1-100 M). Disruption of th endothelium and inhibition of cyclooxygenase (COX) by indomethacin produced identical attenuation of vasodilation to H 2O2. Conversely, the vasodilation to H 2O2 was not affected by either the NO synthase inhibitor N G -nitro-L-arginine methyl ester or the cytochrome P-450 enzyme blocker miconazole. Inhibition of the COX-1, but not the COX-2 pathway, attenuated H 2O2-induced dilation similarly to indomethacin. The production of prostaglandin E 2 (PGE2), but not prostaglandin I2, from coronary arterioles was significantly increased by H 2O2. Furthermore, inhibition of PGE 2 receptors with AH-6809 attenuated vasodilation to H 2O2 similar to that produced by indomethacin. In the absence of a functional endothelium, H 2O2-induced dilation was attenuated, in an identical manner, by a depolarizing agent KCl and a calcium-activated potassium (K Ca) channel inhibitor iberiotoxin. However, PGE 2-induced dilation was not affected by iberiotoxin. The endothelium-independent dilation to H 2O2 was also insensitive to the inhibition of guanylyl cyclase, lipoxygenase, ATP-sensitive potassium channels, and inward rectifier potassium channels. These results suggest that H 2O2 induces endothelium-dependent vasodilation through COX-1-mediated release of PGE 2 and also directly relaxes smooth muscle by hyperpolarization through K Ca channel activation. oxidative stress; prostaglandins; smooth muscle; hyperpolarization

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“…Among the various biological effects attributed to ROS, vascular endothelial dysfunction has consistently been noted, irrespective of the preparations used. 2,18) In addition, ROS generated by the XϩXOD system caused contraction of rat pulmonary artery 19) and canine basilar artery, 20) whereas it relaxed canine coronary artery, 21) implying the existence of species or tissue differences in response to ROS. Furthermore, the responses of arteries to ROS are well-known to be influenced by the presence of endothelium.…”

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confidence: 99%

Sustained Contraction and Endothelial Dysfunction Induced by Reactive Oxygen Species in Porcine Coronary Artery

Ishihara

Sekine

Hatano

et al. 2008

Biological & Pharmaceutical Bulletin

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Reactive oxygen species (ROS), including superoxide anions, hydrogen peroxide and hydroxyl radicals, can be produced in vivo by mechanisms related to mitochondrial respiration, xanthine oxidase (XOD), nitric oxide synthase (NOS), NADPH oxidase, and arachidonic acid metabolism.1,2) Disruption to one or more of these mechanisms is thought to be responsible for the pathogenesis of various diseases. [3][4][5][6] Of these mechanisms, XOD may be involved in the generation of ROS in the endothelium during ischemia and/or reperfusion. 7,8) Roy and McCord demonstrated that xanthine dehydrogenase is proteolytically converted to XOD in tissues within seconds or minutes of an ischemic episode, depending on the tissue involved. 9) Although both enzymes are involved in the catabolism of purine compounds, the latter transfers electrons to molecular oxygen to yield the ROS, superoxide anions and hydrogen peroxide. 10,11) Thus, the deleterious effects of reoxygenation or reperfusion in ischemic tissues can therefore be explained on the basis of the ROS produced by the xanthine-XOD (XϩXOD) system. For a better understanding of the pathogenesis of tissue damage by ROS, it is important to clarify which species of oxygen intermediates are involved in these events, and whether or not there are differences in sensitivity to ROS among various tissues.The direct effects of ROS on cultured vascular endothelial cells or isolated, perfused tissues have been extensively investigated, either by using ROS directly, or using a ROS-generating system, such as the XϩXOD system. [12][13][14][15][16][17] In these studies, ROS scavengers are used to clarify the species of ROS involved in these effects. Among the various biological effects attributed to ROS, vascular endothelial dysfunction has consistently been noted, irrespective of the preparations used. 2,18) In addition, ROS generated by the XϩXOD system caused contraction of rat pulmonary artery 19) and canine basilar artery, 20) whereas it relaxed canine coronary artery, 21) implying the existence of species or tissue differences in response to ROS. Furthermore, the responses of arteries to ROS are well-known to be influenced by the presence of endothelium. 12,13,16) Thus, the responses of the vasculature, including the endothelium, to ROS are complex, and the sensitivity to ROS probably varies depending on the tissue involved. Disruption to the functional integrity of blood vessels will inevitably alter the function of the organ supplied by these vessels. Thus, in the present study, we directed our attention to the effects of ROS on porcine coronary artery, in terms of muscular and endothelial functions, and attempted to determine characteristics of the responses of each vascular element, and to clarify the specific ROS involved. MATERIALS AND METHODS Preparation of Coronary Arterial RingsPorcine hearts, immersed in ice-cooled saline, were transported to the laboratory from an abattoir, usually within 1 h of death. The left anterior descending coronary artery was isolated 2-3 cm from its orig...

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Reactive oxygen species alter contractile properties of pulmonary arterial smooth muscle

Cited by 103 publications

References 20 publications

Hydrogen peroxide-induced Ca²⁺mobilization in pulmonary arterial smooth muscle cells

Hydrogen peroxide-induced Ca²⁺mobilization in pulmonary arterial smooth muscle cells

Hydrogen peroxide induces endothelium-dependent and -independent coronary arteriolar dilation: role of cyclooxygenase and potassium channels

Sustained Contraction and Endothelial Dysfunction Induced by Reactive Oxygen Species in Porcine Coronary Artery

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Reactive oxygen species alter contractile properties of pulmonary arterial smooth muscle

Cited by 103 publications

References 20 publications

Hydrogen peroxide-induced Ca2+mobilization in pulmonary arterial smooth muscle cells

Hydrogen peroxide-induced Ca2+mobilization in pulmonary arterial smooth muscle cells

Hydrogen peroxide induces endothelium-dependent and -independent coronary arteriolar dilation: role of cyclooxygenase and potassium channels

Sustained Contraction and Endothelial Dysfunction Induced by Reactive Oxygen Species in Porcine Coronary Artery

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Hydrogen peroxide-induced Ca²⁺mobilization in pulmonary arterial smooth muscle cells

Hydrogen peroxide-induced Ca²⁺mobilization in pulmonary arterial smooth muscle cells