Coronary artery constriction by the isoprostane 8‐epi prostaglandin F<sub>2α</sub>

Kromer, Brendan M.; Tippins, John R.

doi:10.1111/j.1476-5381.1996.tb16033.x

Cited by 132 publications

(93 citation statements)

References 19 publications

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“…salt loading increased urinary 8-isoprostane excretion, which was counteracted by L-arginine supplementation ( Figure 7A). Isoprostane can exert potent biological activity such as vasoconstriction, 48 stimulate thromboxane receptors, and contribute to atherosclerotic lesion development. 49 Enhanced formation of 8-isoprostane has been associated with several cardiovascular risk factors 50 and has been found to correlate with in vivo thromboxane A 2 biosynthesis.…”

Section: Discussionmentioning

confidence: 99%

l -Arginine Reverses p47phox and gp91phox Expression Induced by High Salt in Dahl Rats

et al. 2003

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Abstract-Derangements in the production and degradation of reactive oxygen species (ROS) as well as nitric oxide (NO) have been implicated in cardiovascular diseases. We explored how supplementation with L-arginine, an NO synthase substrate, restores such derangements of ROS/NO systems in Dahl salt-sensitive, hypertensive (DS) rats. We detected an increase of NADPH oxidase activity, a key enzyme that produces superoxide, in the membrane fraction of the renal cortex derived from DS rats loaded with high salt for 4 weeks; high salt loading also remarkably increased urinary H 2 O 2 , 8-isoprostane, and thromboxane B 2 excretion and decreased plasma NO end products. These changes from high salt loading were counteracted by oral L-arginine supplementation. We further examined expression patterns of NADPH oxidase subunits in renal cortex derived from these animals. High salt loading increased gp91phox and p47phox but not p22phox or Rac1 or mRNA abundance, which were counteracted with L-arginine supplementation. Western blot analyses after subcellular fractionation revealed that L-arginine supplementation distinctly decreases membrane localization of p47phox protein, as it decreases total expression of Rac1 protein in DS rats with high salt loading. These results disclose that high salt loading causes a deficiency in available L-arginine amounts for NO synthases and induces NADPH oxidase activation in the renal cortex of DS rats, which L-arginine supplementation markedly restores. Since superoxide rapidly eliminates NO, which inhibits sodium reabsorption in the cortical collecting duct, superoxide production caused by upregulated NADPH oxidase activity in the renal cortex of high salt-loaded DS rats may accelerate sodium reabsorption and hypertension. Key Words: rats, Dahl Ⅲ arginine Ⅲ hypertension, sodium-dependent Ⅲ nitric oxide Ⅲ cardiovascular diseases R ecent studies have revealed significant associations between the pathogenesis of numerous cardiovascular diseases, including hypertensive states, and the increase in reactive oxygen species (ROS) and/or the decrease in nitric oxide (NO). [1][2][3] Complete understanding of such derangements in ROS/NO systems has been prevented by the fact that mammalian organs are provided with multiple layers of complicated enzymatic as well as nonenzymatic machineries that deal with ROS/NO. 4,5 Among such machineries, NADPH oxidase, which was originally known to produce a large amount of superoxide anion to kill bacteria in neutrophils, 6 has attracted much attention as a potentially important player in a wide array of cardiovascular disorders. Although NADPH oxidase in the nonphagocytic cells has been less well characterized, physiologically relevant low generation of ROS and neutrophillike expression of NADPH oxidase subunits is present in vascular tissues, 7,8 which is activated by pulsatile stretch, 9 platelet-derived growth factor, 10 and angiotensin II. 1,[11][12][13][14][15] These studies, when taken together, suggest that NADPH oxidase may exert broader actions in cardi...

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Section: Discussionmentioning

confidence: 99%

l -Arginine Reverses p47phox and gp91phox Expression Induced by High Salt in Dahl Rats

et al. 2003

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“…Concentrations of the isoprostane, 8-epi-prostaglandin(PG)F 2a , are raised in the plasma of non-insulin-dependent diabetic subjects [19] and in heavy smokers [20]. In addition, 8-epi-PGF 2a is a potent constrictor of the coronary circulation [21].…”

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Dietary antioxidant supplementation reduces lipid peroxidation but impairs vascular function in small mesenteric arteries of the streptozotocin-diabetic rat

et al. 1998

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Insulin-dependent diabetes mellitus (IDDM) is associated with abnormal function of the vascular endothelium and it is proposed that this defect could underlie many of the associated vasculopathies [1]. Studies from our laboratory and others have reported impaired vasodilatory responses to the endothelium-dependent vasodilator acetylcholine (ACh) in isolated arteries from diabetic subjects [2] and in mesenteric [3], femoral [4] and aortic [5] arteries from the streptozotocin (STZ)-diabetic rat (an animal model of uncontrolled IDDM). Although a physiological endothelium-dependent dilatory role of ACh has sometimes been questioned, the reduced relaxation of arteries from diabetic animals to other endothelium-dependent dilators [1] and to increasing luminal flow [6] would suggest that the poor ACh responses reflect a generalised endothelial defect. The abnormal ACh response is likely to result from either decreased nitric oxide (NO) synthesis or increased NO degradation [3,4]. Several mechanisms have been hypothesised, among which is the suggestion that oxidative stress could play an important role [7,8]. Diabetologia (1998) Summary Impaired endothelium-dependent relaxation could underlie many of the vascular complications associated with insulin-dependent diabetes mellitus, and may be mediated by increased oxidative stress. The effect of antioxidants on vascular endothelial function and oxidative stress of streptozotocin-diabetic rats was assessed by dietary supplementation with vitamins E and C. Diabetic (i. v. streptozotocin, 45 mg/kg) male Sprague-Dawley rats were fed one of six supplemented diets containing 75.9, 250, or 500 mg vitamin E/kg chow, 250 mg vitamin C/kg H 2 0, 250 mg vitamin E/kg chow plus 250 mg vitamin C/kg H 2 O, or chow deficient in vitamin E, and then compared to standard-fed control rats. After 4 weeks, small mesenteric arteries were dissected and mounted on a small vessel myograph, concentration response curves were then constructed to noradrenaline, acetylcholine and sodium nitroprusside. Acetylcholinemediated relaxation was impaired in arteries from diabetic rats (pEC 50 6.701 ± SEM 0.120, n = 8) compared to controls (7.386 ± 0.078, n = 6; p < 0.05). The 500 mg/kg vitamin E diet further impaired maximum relaxation to acetylcholine (58.2 ± 10.5 vitamin E, n = 7 vs 84.4 ± 5.3 % standard, p < 0.05), and the combined vitamin E plus C diet impaired maximum relaxation to sodium nitroprusside (48.5 ± 4.1 in vitamin E + C, n = 8 vs 75.6 ± 3.9 % standard; p < 0.01). However, plasma 8-epi-prostaglandin (PG)F 2 a (measured as an estimate of oxidative stress) was dose-dependently decreased in rats on vitamin E supplemented diets. Dietary antioxidant supplementation did not reverse impaired endothelial function in this model of uncontrolled diabetes despite a concomitant decrease in oxidative stress. [Diabetologia (1998) 41: 148±156]

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“…Endotoxaemia results in increased production of reactive oxygen species (Blackwell et al, 1996) and LPS induces isoprostane production in vivo (Mcadam et al, 2000). As blood vessels alter their responses to 8-iso PGF 2a after exposure to oxidative (Kromer & Tippins, 1996) or in¯ammatory (Jourdan et al, 1998) stress (c) were performed in parallel. *Illustrates a signi®cant di erence between aggregation in comparison to control response in non-LPS-treated blood using two-way ANOVA.…”

Section: Discussionmentioning

confidence: 99%

“…8-iso PGF 2a causes contraction of isolated blood vessels, (Kromer & Tippins, 1996;Jourdan et al, 1997b;Gardan et al, 2000;Oliviera et al, 2000), lymphatics, and airway (Kawikova et al, 1996) and myometrial smooth muscle (Crankshaw, 1995). Where studied, smooth muscle contraction appears to be mediated in part via thromboxane TP receptors (Fukunaga et al, 1993;Kromer & Tippins, 1996;Jourdan et al, 1997b;Gardan et al, 2000;Oliviera et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Characterization of the effects of isoprostanes on platelet aggregation in human whole blood

Cranshaw

Evans

Mitchell

2001

British J Pharmacology

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1 We tested the e ects of 11 commercially-available isoprostanes on platelet aggregation directly or when triggered by the thromboxane receptor agonist U46619 or collagen in healthy human citrated blood using a whole blood aggregometer.2 None of the isoprostanes tested triggered aggregation alone, nor facilitated aggregation by a subthreshold dose of U46619 or collagen. Five isoprostanes inhibited aggregation (rank order of potency 8-iso PGE 1 48-iso PGE 2 48-iso PGF 2a 48-iso PGF 3a 48-iso-13,14-dihydro-15-keto PGF 2a ). 3 Blood incubated with LPS to induce a gross in¯ammatory response exhibited a time dependent (2 ± 12 h) reduction in aggregation to U46619 but maintained a consistent response to collagen. Under these conditions, as in control blood, none of the isoprostanes tested induced aggregation. In fact, the inhibitory actions of isoprostanes on U46619-induced aggregation were enhanced in blood treated with LPS. 4 L-NAME inhibited aggregation induced by U46619 in fresh blood and in blood treated with LPS. In the presence of L-NAME, (with or without LPS) none of the isoprostanes tested induced aggregation but retained their inhibitory action. 5 Thus, in human whole blood the action of 8-iso PGE 1 , 8-iso PGE 2 , 8-iso PGF 2a , 8-iso PGF 3a , and 8-iso-13,14-dihydro-15-keto PGF 2a is antiaggregatory. Moreover, this inhibitory capacity is still apparent and may be enhanced in blood subjected to in¯ammatory stimulation.

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Coronary artery constriction by the isoprostane 8‐epi prostaglandin F_2α

Cited by 132 publications

References 19 publications

l -Arginine Reverses p47phox and gp91phox Expression Induced by High Salt in Dahl Rats

l -Arginine Reverses p47phox and gp91phox Expression Induced by High Salt in Dahl Rats

Dietary antioxidant supplementation reduces lipid peroxidation but impairs vascular function in small mesenteric arteries of the streptozotocin-diabetic rat

Characterization of the effects of isoprostanes on platelet aggregation in human whole blood

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Coronary artery constriction by the isoprostane 8‐epi prostaglandin F2α

Cited by 132 publications

References 19 publications

l -Arginine Reverses p47phox and gp91phox Expression Induced by High Salt in Dahl Rats

l -Arginine Reverses p47phox and gp91phox Expression Induced by High Salt in Dahl Rats

Dietary antioxidant supplementation reduces lipid peroxidation but impairs vascular function in small mesenteric arteries of the streptozotocin-diabetic rat

Characterization of the effects of isoprostanes on platelet aggregation in human whole blood

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Coronary artery constriction by the isoprostane 8‐epi prostaglandin F_2α