Pharmacological nature of nicotine-induced contraction in the rat basilar artery: Involvement of arachidonic acid metabolites

Ji, Xu; Nishihashi, Tsuyoshi; Trandafir, Cristina C.; Wang, Aimin; Shimizu, Yuma; Kurahashi, Kazuyoshi

doi:10.1016/j.ejphar.2007.08.011

Cited by 20 publications

(10 citation statements)

References 28 publications

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“…Consistent with that finding, it has been demonstrated that inhibiting iPLA 2 with BEL inhibits agonist-induced smooth muscle contraction in various blood vessels that include rabbit portal veins (15), rabbit carotid artery (16), rat basilar artery (17), and mouse cerebral and mesenteric arteries (16). Whether iPLA 2 ␤ participates in diabetes-associated vascular smooth muscle hypercontractility is not yet known, but we demonstrate here that iPLA 2 activity and iPLA 2 ␤ protein expression are increased in aortae and mesentery arteries isolated from animal models of type 1 (STZ mice or rats) and type 2 (db/db mice) diabetes.…”

Section: Discussionsupporting

confidence: 58%

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Role of Calcium-independent Phospholipase A2β in High Glucose-induced Activation of RhoA, Rho Kinase, and CPI-17 in Cultured Vascular Smooth Muscle Cells and Vascular Smooth Muscle Hypercontractility in Diabetic Animals

Xie

Gong

et al. 2010

Journal of Biological Chemistry

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Previous studies suggest that high glucose-induced RhoA/ Rho kinase/CPI-17 activation is involved in diabetes-associated vascular smooth muscle hypercontractility. However, the upstream signaling that links high glucose and RhoA/Rho kinase/ CPI-17 activation is unknown. Here we report that calciumindependent phospholipase A 2 ␤ (iPLA 2 ␤) is required for high glucose-induced RhoA/Rho kinase/CPI-17 activation and thereby contributes to diabetes-associated vascular smooth muscle hypercontractility. We demonstrate that high glucose increases iPLA 2 ␤ mRNA, protein, and iPLA 2 activity in a timedependent manner. Protein kinase C is involved in high glucoseinduced iPLA 2 ␤ protein up-regulation. Inhibiting iPLA 2 ␤ activity with bromoenol lactone or preventing its expression by genetic deletion abolishes high glucose-induced RhoA/Rho kinase/CPI-17 activation, and restoring expression of iPLA 2 ␤ in iPLA 2 ␤-deficient cells also restores high glucose-induced CPI-17 phosphorylation. Pharmacological and genetic inhibition of 12/15-lipoxygenases has effects on high glucose-induced CPI-17 phosphorylation similar to iPLA 2 ␤ inhibition. Moreover, increases in iPLA 2 activity and iPLA 2 ␤ protein expression are also observed in both type 1 and type 2 diabetic vasculature. Pharmacological and genetic inhibition of iPLA 2 ␤, but not iPLA 2 ␥, diminishes diabetes-associated vascular smooth muscle hypercontractility. In summary, our results reveal a novel mechanism by which high glucose-induced, protein kinase C-mediated iPLA 2 ␤ up-regulation activates the RhoA/Rho kinase/CPI-17 via 12/15-lipoxygenases and thereby contributes to diabetes-associated vascular smooth muscle hypercontractility.The prevalence of diabetes has increased dramatically in the United States and worldwide. Diabetes-associated microvascular and macrovascular complications are the major causes of increased mortality and morbidity in diabetic patients (1). It is recognized that abnormal vascular reactivity, including an increase in vasoconstrictive responses and/or a decrease in vasodilatory responses, are present early in diabetes, and this might contribute to the development of diabetes-associated vascular complications (2). Although diabetes-associated endothelial and vasodilatatory dysfunction has been studied extensively, much less is known about vascular smooth muscle dysfunction in diabetes, and the molecular mechanisms that underlie endothelium-independent, diabetes-associated vascular smooth muscle hypercontractility are largely unknown.G-protein-coupled receptor agonists can induce significant smooth muscle contraction by inhibiting myosin light chain phosphatase at a given Ca 2ϩ concentration by a mechanism designated "Ca 2ϩ sensitization" (3). A small GTP-binding protein RhoA, its downstream effector Rho kinase (ROCK), 2 protein kinase C (PKC), and CPI-17 (protein kinase C-potentiated phosphatase inhibitor of 17 kDa) are recognized as four key participants in Ca 2ϩ sensitization of vascular smooth muscle contraction (4). Importantly, abnormal act...

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Section: Discussionsupporting

confidence: 58%

“…Using this pharmacological inhibitor, previous studies suggest that iPLA 2 is involved in agonist-induced smooth muscle contraction (15)(16)(17). Although the mechanism by which iPLA 2 mediates smooth muscle contraction remains elusive, Maeda et al (18) reported that inhibiting iPLA 2 with BEL inhibits thrombin-induced ROCK activation in endothelial cells.…”

mentioning

confidence: 99%

Role of Calcium-independent Phospholipase A2β in High Glucose-induced Activation of RhoA, Rho Kinase, and CPI-17 in Cultured Vascular Smooth Muscle Cells and Vascular Smooth Muscle Hypercontractility in Diabetic Animals

Xie

Gong

et al. 2010

Journal of Biological Chemistry

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“…Application of indomethacin removes the ACh-induced contractions thus highlighting a role for COX involvement in the generation of EDCF. Further analysis shows that ketoprofen (at a pharmacological concentration reported to produce effective inhibition [43,44]) was without influence on the contraction induced by ACh, suggesting that COX-1 has no involvement.…”

Section: Discussionmentioning

confidence: 97%

Endothelium-derived contraction in a model of rheumatoid arthritis is mediated via angiotensin II type 1 receptors

Hamilton

Dunning

Ferrell

et al. 2018

Vascular Pharmacology

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A role for endothelium-derived constricting factors (EDCF), and the angiotensin II type 1 receptor (AT1R) pathway, in the vascular impairment found in the rat Freund's complete adjuvant (FCA)-model of rheumatoid arthritis (RA) was examined. FCA arthritis was induced in rats±losartan. Vehicle-treated rats served as controls. Knee-joint swelling and red blood cell (RBC) aggregation were measured as indicators of inflammation and endothelium reactivity assessed by response to acetylcholine (ACh) on aortic rings. Results show that knee-joint swelling and RBC aggregation were elevated in the FCA+vehicle group and restored to control levels in the FCA+losartan-treated animals. ACh-induced relaxation of aortic rings taken from FCA+vehicle animals was significantly impaired compared to vehicle-controls and this vasoreactivity was restored to control levels in the FCA+losartan-treated group. Further examination of aorta from the FCA+vehicle animals revealed an EDCF that was reliant on cyclooxygenase-2 (but not cyclooxygenase-1), generation of superoxide anion generation (but not hydrogen peroxide) and activation of thromboxane-prostanoid receptor. Losartan administration in vivo or ex vivo (to aortic rings) prevented the generation of the EDCF. In summary, this is the first evidence of an EDCF in a model of RA and identifies this mechanism as potentially significant in the cardiovascular disorder associated with the disease.

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“…However, trehalose did not directly inhibit the enzyme activity of cPLA 2 , despite a decrease in production of lipid mediators and arachidonic acid release induced by hemolysate treatment in cultured cells. The Ca 2+ -independent PLA 2 (iPLA 2 , group VI PLA 2 ) is involved in arachidonic acid release induced by various stimulations and nicotine-induced contraction in the basilar artery via arachidonic acid metabolites [33,34]. Thus, iPLA 2 may be involved in arachidonic acid release and vasospasm induced by blood, and trehalose may suppress the enzyme activity of iPLA 2 .…”

Section: Discussionmentioning

confidence: 99%

Trehalose treatment suppresses inflammation, oxidative stress, and vasospasm induced by experimental subarachnoid hemorrhage

et al. 2012

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BackgroundSubarachnoid hemorrhage (SAH) frequently results in several complications, including cerebral vasospasm, associated with high mortality. Although cerebral vasospasm is a major cause of brain damages after SAH, other factors such as inflammatory responses and oxidative stress also contribute to high mortality after SAH. Trehalose is a non-reducing disaccharide in which two glucose units are linked by α,α-1,1-glycosidic bond, and has been shown to induce tolerance to a variety of stressors in numerous organisms. In the present study, we investigated the effect of trehalose on cerebral vasospasm, inflammatory responses, and oxidative stress induced by blood in vitro and in vivo.MethodsEnzyme immunoassay for eicosanoids, pro-inflammatory cytokines, and endothelin-1, and western blotting analysis for cyclooxygenase-2, inducible nitric oxide synthase, and inhibitor of NF-κB were examined in macrophage-like cells treated with hemolysate. After treatment with hemolysate and hydrogen peroxide, the levels of lipid peroxide and amounts of arachidonic acid release were also analyzed. Three hours after the onset of experimental SAH, 18 Japanese White rabbits received an injection of saline, trehalose, or maltose into the cisterna magna. Angiographic and histological analyses of the basilar arteries were performed. In a separate study, the femoral arteries from 60 rats were exposed to fresh autologous blood. At 1, 3, 5, 7, 10, and 20 days after treatment, cryosections prepared from the femoral arteries were histologically analyzed.ResultsWhen cells were treated with hemolysate, trehalose inhibited the production of several inflammatory mediators and degradation of the inhibitor of NF-κB and also suppressed the lipid peroxidation, the reactive oxygen species-induced arachidonic acid release in vitro. In the rabbit model, trehalose produced an inhibitory effect on vasospasm after the onset of experimental SAH, while maltose had only a moderate effect. When the rat femoral arteries exposed to blood were investigated for 20 days, histological analysis revealed that trehalose suppressed vasospasm, inflammatory response, and lipid peroxidation.ConclusionsThese data suggest that trehalose has suppressive effects on several pathological events after SAH, including vasospasm, inflammatory responses, and lipid peroxidation. Trehalose may be a new therapeutic approach for treatment of complications after SAH.

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Pharmacological nature of nicotine-induced contraction in the rat basilar artery: Involvement of arachidonic acid metabolites

Cited by 20 publications

References 28 publications

Role of Calcium-independent Phospholipase A2β in High Glucose-induced Activation of RhoA, Rho Kinase, and CPI-17 in Cultured Vascular Smooth Muscle Cells and Vascular Smooth Muscle Hypercontractility in Diabetic Animals

Role of Calcium-independent Phospholipase A2β in High Glucose-induced Activation of RhoA, Rho Kinase, and CPI-17 in Cultured Vascular Smooth Muscle Cells and Vascular Smooth Muscle Hypercontractility in Diabetic Animals

Endothelium-derived contraction in a model of rheumatoid arthritis is mediated via angiotensin II type 1 receptors

Trehalose treatment suppresses inflammation, oxidative stress, and vasospasm induced by experimental subarachnoid hemorrhage

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