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

Christine L. Oltman, Neal L. Kane, Francis J. Miller, Arthur A. Spector, Neal L. Weintraub, Kevin C. Dellsperger

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

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 O 2 - scavenger), 250 U/ml PEG-catalase (a H 2 O 2 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 [ 3 H]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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume285
Issue number6 54-6
StatePublished - Dec 1 2003
Externally publishedYes

Fingerprint

Microvessels
Arachidonic Acid
Dilatation
Reactive Oxygen Species
Swine
Polyethylene
Indomethacin
1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt
Catalase
Diclofenac
Vasodilation
Video Microscopy
Cyclooxygenase Inhibitors
Endothelins
Arterioles
Microcirculation
Prostaglandin-Endoperoxide Synthases
Oxidants
Constriction
Superoxide Dismutase

Keywords

  • Coronary microcirculation
  • Cyclooxygenase

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Reactive oxygen species mediate arachidonic acid-induced dilation in porcine coronary microvessels. / Oltman, Christine L.; Kane, Neal L.; Miller, Francis J.; Spector, Arthur A.; Weintraub, Neal L.; Dellsperger, Kevin C.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 285, No. 6 54-6, 01.12.2003.

Research output: Contribution to journalArticle

Oltman, Christine L. ; Kane, Neal L. ; Miller, Francis J. ; Spector, Arthur A. ; Weintraub, Neal L. ; Dellsperger, Kevin C. / Reactive oxygen species mediate arachidonic acid-induced dilation in porcine coronary microvessels. In: American Journal of Physiology - Heart and Circulatory Physiology. 2003 ; Vol. 285, No. 6 54-6.
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