Reactive Oxygen Species: Role in the Relaxation Induced by Bradykinin or Arachidonic Acid Via EDHF in Isolated Porcine Coronary Arteries

1999 ◽  
Vol 34 (4) ◽  
pp. 567-574 ◽  
Author(s):  
Silvia Pomposiello ◽  
Nour-Eddine Rhaleb ◽  
Magaly Alva ◽  
Oscar A. Carretero
Keyword(s):  
Reactive Oxygen Species ◽  
Arachidonic Acid ◽  
Coronary Arteries ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Reactive oxygen species mediate arachidonic acid-induced dilation in porcine coronary microvessels

2003 ◽  
Vol 285 (6) ◽  
pp. H2309-H2315 ◽  
Author(s):  
Christine L. Oltman ◽  
Neal L. Kane ◽  
Francis J. Miller ◽  
Arthur A. Spector ◽  
Neal L. Weintraub ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Arachidonic Acid ◽  
Coronary Arteries ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cox Inhibitors ◽  
Ros Scavenger ◽  
Krebs Buffer

Reactive oxygen species (ROS) have been proposed to mediate vasodilation in the microcirculation. We investigated the role of ROS in arachidonic acid (AA)-induced coronary microvascular dilation. Porcine epicardial coronary arterioles (110 ± 4 μm diameter) were mounted onto pipettes in oxygenated Krebs buffer. Vessels were incubated with vehicle or 1 mM Tiron (a nonselective ROS scavenger), 250 U/ml polyethylene-glycolated (PEG)-superoxide dismutase (SOD; an [Formula: see text] scavenger), 250 U/ml PEG-catalase (a H2O2 scavenger), or the cyclooxygenase (COX) inhibitors indomethacin (10 μM) or diclofenac (10 μM) for 30 min. After endothelin constriction (30–60% of resting diameter), cumulative concentrations of AA (10–10–10–5 M) were added and internal diameters measured by video microscopy. AA (10–7 M) produced 37 ± 6% dilation, which was eliminated by the administration of indomethacin (4 ± 7%, P < 0.05) or diclofenac (–8 ± 8%, P < 0.05), as well as by Tiron (–4 ± 5%, P < 0.05), PEG-SOD (–10 ± 6%, P < 0.05), or PEG-catalase (1 ± 4%, P < 0.05). Incubation of small coronary arteries with [3H]AA resulted in the formation of prostaglandins, which was blocked by indomethacin. In separate studies in microvessels, AA induced concentration-dependent increases in fluorescence of the oxidant-sensitive probe dichlorodihydrofluorescein diacetate, which was inhibited by pretreatment with indomethacin or by SOD + catalase. We conclude that in porcine coronary microvessels, COX-derived ROS contribute to AA-induced vasodilation.

scholarly journals Arachidonic acid- and prostaglandin E2-induced cerebral vasodilation is mediated by carbon monoxide, independent of reactive oxygen species in piglets

2011 ◽  
Vol 301 (6) ◽  
pp. H2482-H2487 ◽  
Author(s):  
Alie Kanu ◽  
Charles W. Leffler
Keyword(s):  
Reactive Oxygen Species ◽  
Carbon Monoxide ◽  
Arachidonic Acid ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Artificial Cerebrospinal Fluid ◽  
Newborn Pigs ◽  
Cerebral Vasodilation ◽  
Prostacyclin Analog ◽  
Cerebral Vascular

Arachidonic acid (AA) and prostaglandin (PG) E2 stimulate carbon monoxide (CO) production, and AA metabolism is known to be associated with the generation of reactive oxygen species (ROS). This study was conducted to address the hypothesis that CO and/or ROS mediate cerebrovascular dilation in newborn pigs. Experiments were performed on anesthetized newborn pigs with closed cranial windows. Different concentrations of AA (10−8-10−6 M), PGE2 (10−8-10−6 M), iloprost (10−8-10−6 M), and their vehicle (artificial cerebrospinal fluid) were given. Piglets with PGE2 and iloprost received indomethacin (5 mg/kg iv) to inhibit cyclooxygenase. AA, PGE2, and iloprost caused concentration-dependent increases in pial arteriolar diameter. The effects of both AA and PGE2 in producing cerebral vascular dilation and associated CO production were blocked by the heme oxygenase inhibitor chromium mesoporphyrin (2 × 10−5 M), but not by the prostacyclin analog, iloprost. ROS inhibitor tempol (SOD mimetic) (1 × 10−5 M) and the H2O2 scavenger catalase (1,000 U/ml) also do not block these vasodilator effects of AA and PGE2. Heme-l-lysinate-induced cerebrovascular dilation and CO production was blocked by chromium mesoporphyrin. Hypoxanthine plus xanthine oxidase, a combination that is known to generate ROS, caused pial arteriolar dilation and CO production that was inhibited by tempol and catalase. These data suggest that AA- and PGE2-induced cerebral vascular dilation is mediated by CO, independent of ROS.

Coronary endothelial dysfunction after cardiomyocyte-specific mineralocorticoid receptor overexpression

2011 ◽  
Vol 300 (6) ◽  
pp. H2035-H2043 ◽  
Author(s):  
Julie Favre ◽  
Ji Gao ◽  
An Di Zhang ◽  
Isabelle Remy-Jouet ◽  
Antoine Ouvrard-Pascaud ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Dysfunction ◽  
Nadph Oxidase ◽  
Coronary Arteries ◽  
Mineralocorticoid Receptor ◽  
Vascular Dysfunction ◽  
Reactive Oxygen ◽  
Oxidase Inhibitor ◽  
Oxygen Species ◽  
Coronary Endothelial Dysfunction

The deleterious effects of aldosterone excess demonstrated in cardiovascular diseases might be linked in part to coronary vascular dysfunction. However, whether such vascular dysfunction is a cause or a consequence of the changes occurring in the cardiomyocytes is unclear. Moreover, the possible link between mineralocorticoid receptor (MR)-mediated effects on the cardiomyocyte and the coronary arteries is unknown. Thus we used a mouse model with conditional, cardiomyocyte-specific overexpression of human MR (hMR) and observed the effects on endothelial function in isolated coronary segments. hMR overexpression decreased the nitric oxide (NO)-mediated relaxing responses to acetylcholine in coronary arteries (but not in peripheral arteries), and this was prevented by a 1-mo treatment either with an MR antagonist, vitamin E/vitamin C, or a NADPH oxidase inhibitor. hMR overexpression did not affect coronary endothelial NO synthase content nor its level of phosphorylation on serine 1177, but increased cardiac levels of reactive oxygen species, cardiac NADPH oxidase (NOX) activity, and expression of the NOX subunit gp91phox, which was limited to endothelial cells. Thus an increase in hMR activation, restricted to cardiomyocytes, is sufficient to induce a severe coronary endothelial dysfunction. We suggest a new paracrine mechanism by which cardiomyocytes trigger a NOX-dependent, reactive oxygen species-mediated coronary endothelial dysfunction.

scholarly journals Increased NAD(P)H Oxidase and Reactive Oxygen Species in Coronary Arteries After Balloon Injury

2001 ◽  
Vol 21 (5) ◽  
pp. 739-745 ◽  
Author(s):  
Yi Shi ◽  
Rodica Niculescu ◽  
Dian Wang ◽  
Sachin Patel ◽  
Kelly L. Davenpeck ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Coronary Arteries ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Balloon Injury

scholarly journals Involvement of cytosolic phospholipase A2, and the subsequent release of arachidonic acid, in signalling by Rac for the generation of intracellular reactive oxygen species in Rat-2 fibroblasts

2000 ◽  
Vol 348 (3) ◽  
pp. 525-530 ◽  
Author(s):  
Chang-Hoon WOO ◽  
Zee-Won LEE ◽  
Byung-Chul KIM ◽  
Kwon-Soo HA ◽  
Jae-Hong KIM
Keyword(s):  
Reactive Oxygen Species ◽  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Active Form ◽  
Reactive Oxygen ◽  
Cytosolic Phospholipase A2 ◽  
Signalling Pathway ◽  
Oxygen Species ◽  
Cytosolic Phospholipase

Although there have been a number of recent studies on the role of Rac in the generation of reactive oxygen species (ROS), details of the signalling pathway remain unclear. In the present study we analysed the extent to which the activation of cytosolic phospholipase A2 and the resultant release of arachidonic acid (AA) are involved in the Rac-mediated generation of ROS. Transfection of Rat-2 cells with RacV12, a constitutively active form of Rac1, induced elevated levels of ROS, as reflected by increased H2O2-sensitive fluorescence of 2ʹ,7ʹ-dichlorofluorescein. These effects could be blocked by inhibiting phospholipase A2 or 5-lipoxygenase but not by inhibiting cyclo-oxygenase. The application of exogenous AA increased levels of ROS but the effect was dependent on the further metabolism of AA to leukotrienes C4/D4/E4 by 5-lipoxygenase. Indeed, the exogenous application of a mixture of leukotrienes C4/D4/E4 elicited transient elevations in the levels of ROS that were blocked by catalase. These findings indicate that phospholipase A2 and subsequent AA metabolism by 5-lipoxygenase act as downstream mediators in a Rac signalling pathway leading to the generation of ROS.

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