Hydrogen peroxide induces contraction and raises [Ca2+]i in canine cerebral arterial smooth muscle: participation of cellular signaling pathways

Zw, Yang; Zheng, Tao; Wang, J; Zhang, A; Altura, Bella T.

doi:10.1007/s002109900128

Cited by 83 publications

(55 citation statements)

References 37 publications

(46 reference statements)

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“…In contrast, other studies suggest that ROS-induced contraction is independent of intracellular Ca 2ϩ in pulmonary artery (17,18,27). Other possible mechanisms include activation of mitogenactivated protein kinase or tyrosine kinase (17,27,48). The effect of ROS on the Rho/Rho kinase Ca 2ϩ -independent pathway has not been investigated previously.…”

Section: Discussionmentioning

confidence: 98%

“…Several studies have examined the contractile response of arteries to ROS. Superoxide and H 2 O 2 induce vasoconstriction in rat aorta (3,20,29), canine basilar artery (48), and rat pulmonary artery (18). Additionally, our data show that the antioxidant Tempol significantly reduced X/XO-induced contractions and the antioxidant catalase decreased X/XO-induced contractions significantly but to a smaller extent.…”

Section: Discussionmentioning

confidence: 99%

“…ROS increase the intracellular Ca 2ϩ concentration via activation of voltagesensitive Ca 2ϩ channels, leading to an influx of extracellular Ca 2ϩ . Removal of extracellular Ca 2ϩ or administration of Ca 2ϩ channel blockers markedly reduces the contraction induced by exogenous ROS (3,48). In addition, ROS release Ca 2ϩ from intracellular stores by inhibiting Ca 2ϩ -ATPase activity and promoting inositol triphosphate-induced Ca 2ϩ release (13,14).…”

Section: Discussionmentioning

confidence: 99%

“…Many studies have shown that ROS increase the tone of arteries by reducing NO bioavailability and endothelium-dependent relaxation (5, 19). However, ROS also contract vessels after removal of endothelium, suggesting that ROS have direct effects on smooth muscle (3,29,48). Although accumulating evidence suggests that ROS can function as second messengers to activate multiple intracellular signal cascades, the mechanisms of ROS-induced vasoconstriction are still incompletely understood and the effects of ROS on the Rho/Rho kinase Ca 2ϩ -independent signaling pathway have not been investigated.…”

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confidence: 99%

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Activation of Rho/Rho kinase signaling pathway by reactive oxygen species in rat aorta

Jin

Zhao

Webb

2004

American Journal of Physiology-Heart and Circulatory Physiology

224

185

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. Activation of Rho/Rho kinase signaling pathway by reactive oxygen species in rat aorta. Am J Physiol Heart Circ Physiol 287: H1495-H1500; 2004; 10.1152/ajpheart.01006.2003.-Evidence indicates that both the Rho/ Rho kinase signaling pathway and reactive oxygen species (ROS) such as superoxide and H 2O2 are involved in the pathogenesis of hypertension. This study aimed to determine whether ROS-induced vascular contraction is mediated through activation of Rho/Rho kinase. Rat aortic rings (endothelium denuded) were isolated and placed in organ chambers for measurement of isometric force development. ROS were generated by a xanthine (X)-xanthine oxidase (XO) mixture. The antioxidants tempol (3 mM) and catalase (1,200 U/ml) or the XO inhibitor allopurinol (400 M) significantly reduced X/XOinduced contraction. A Rho kinase inhibitor, (ϩ)-(R)-trans-4-(1-aminoethyl-N-4-pyridil)cyclohexanecarboxamide dihydrochloride (Y-27632), decreased the contraction in a concentration-dependent manner; however, the Ca 2ϩ -independent protein kinase C inhibitor rottlerin did not have an effect on X/XO-induced contraction. Phosphorylation of the myosin light chain phosphatase target subunit (MYPT1) was increased by ROS, and preincubation with Y-27632 blocked this increased phosphorylation. Western blotting for cytosolic and membrane-bound fractions of Rho showed that Rho was increased in the membrane fraction by ROS, suggesting activation of Rho. These observations demonstrate that ROS-induced Ca 2ϩ sensitization is through activation of Rho and a subsequent increase in Rho kinase activity but not Ca 2ϩ -independent PKC. myosin light chain phosphatase; smooth muscle contraction; antioxidants CONTRACTION OF SMOOTH MUSCLE is regulated by both Ca 2ϩ -dependent and Ca 2ϩ -independent (Ca 2ϩ sensitization) mechanisms. A rise in intracellular Ca 2ϩ levels leads to myosin light chain (MLC) kinase activation, resulting in an increase in MLC phosphorylation. Importantly, MLC phosphorylation can also be increased through inhibition of MLC phosphatase, which augments smooth muscle force generation without a change in intracellular Ca 2ϩ (38).In recent years, studies have revealed that the small GTPase Rho and its downstream target Rho kinase mediate the Ca 2ϩ sensitization of smooth muscle contraction (37). The exchange of bound GDP for GTP activates Rho and stimulates its translocation from cytosol to membrane. Rho-GTP phosphorylates Rho kinase, which inhibits MLC phosphatase activity by phosphorylation of the MLC phosphatase target subunit (MYPT1). A decrease in MLC phosphatase activity increases phosphorylation of myosin and therefore contributes to smooth muscle contraction at low levels of intracellular Ca 2ϩ concentration. Strong evidence suggests that increased Rho/Rho kinase-dependent Ca 2ϩ sensitization contributes to hypertension and inhibition of Rho or Rho kinase reduces blood pressure (33, 42). Some heterotrimetric G protein-coupled receptor (GPCR) agonists, including angiotensin II (ANG II) and endothelin (ET)-1, induce smooth mus...

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Activation of Rho/Rho kinase signaling pathway by reactive oxygen species in rat aorta

Jin

Zhao

Webb

2004

American Journal of Physiology-Heart and Circulatory Physiology

224

185

View full text Add to dashboard Cite

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“…3 In the present study, exposure of basilar arteries to H 2 O 2 resulted in loss of endotheliumdependent relaxation in response to substance P and marked disruption of the endothelial layer, supporting the cytotoxicity of H 2 O 2 in endothelial cells. 1,2,7,9,11 Exogenous H 2 O 2 increases intracellular calcium and depletes cellular adenosine triphosphate, 2,7,22 which may result in morphological changes in endothelial cells. 7 Exposure to H 2 O 2 also inhibited the endothelium-independent relaxation response to SNP and the contractile response to KCl and PGF 2α in basilar arteries, suggesting that vascular smooth muscle cells are also involved in H 2 O 2 -induced vascular injury.…”

Section: Discussionmentioning

confidence: 99%

Halothane does not protect against vascular injury in isolated cerebral and mesenteric arteries

Ogawa

Tokinaga

Iwahashi

et al. 2005

Can J Anesth/J Can Anesth

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Purpose: This study was designed to examine regional differences in the vascular injury induced by hydrogen peroxide (H 2 O 2 ), and to determine its modulation by halothane in canine basilar and mesenteric arteries. Methods:Rings of canine basilar and mesenteric arteries with intact endothelium were mounted in Krebs bicarbonate solution for isometric tension recording. The relaxation responses to substance P (10 -8 M) and sodium nitroprusside (SNP; 10 -8 to 10 -5 M) were examined before and after exposure to H 2 O 2 (1 mM) for eight minutes in the presence or absence of halothane (2%), to evaluate the effects of oxidative injury on the endothelium-dependent and -independent relaxation. The contractile responses to KCl (30 mM) and prostaglandin (PG) F 2α (3 × 10 -6 M) were also compared in rings with and without exposure to H 2 O 2 . Results: After exposure to H 2 O 2 , the relaxant responses to substance P were significantly inhibited in basilar arteries (P < 0.01), but not in mesenteric arteries. Exposure to H 2 O 2 also attenuated SNP-induced relaxation in basilar (P < 0.05), but not in mesenteric arteries. The attenuation of the contractile responses to KCl and PGF 2α after H 2 O 2 exposure was observed only in basilar arteries (P < 0.01). Simultaneous exposure to halothane did not affect the attenuation of these relaxant and contractile responses. Scanning electron microscopy revealed that H 2 O 2 resulted in marked disruption of the endothelial layer in basilar arteries, compared to almost no morphological changes in mesenteric arteries. Conclusion:These results indicate that the endothelium and vascular smooth muscle of the basilar artery are more susceptible to oxidative stress than those of the mesenteric artery. Halothane, at clinically relevant concentrations, exerts no significant influence on this vascular injury. Objectif

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Hydrogen Peroxide Regulates Metaplasticity in the Hippocampus

Kamsler

Segal

2005

Synaptic Plasticity and Transsynaptic Signaling

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Hydrogen peroxide induces contraction and raises [Ca2+]i in canine cerebral arterial smooth muscle: participation of cellular signaling pathways

Cited by 83 publications

References 37 publications

Activation of Rho/Rho kinase signaling pathway by reactive oxygen species in rat aorta

Activation of Rho/Rho kinase signaling pathway by reactive oxygen species in rat aorta

Halothane does not protect against vascular injury in isolated cerebral and mesenteric arteries

Hydrogen Peroxide Regulates Metaplasticity in the Hippocampus

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