Interactions of Volatile Anesthetics and Reactive Oxygen Intermediates on Vascular Smooth Muscle

Effects of reactive oxygen intermediates generated by hypoxanthine plus xanthine oxidase on the Ca(2+)-adenosinetriphosphatase (ATPase) of sarcoplasmic reticulum from bovine aortic smooth muscle were studied. Exogenous hypoxanthine (0.1-100 microM) plus xanthine oxidase (10 mU/ml) produced an hypoxanthine concentration-dependent inhibition of the Ca(2+)-ATPase. The inhibition could be completely blocked by superoxide dismutase (100 U/ml) but not by either mannitol (20 mM) or deferoxamine (100 microM). Direct addition of hydrogen peroxide in the micromolar range did not cause significant inhibition. These results suggest that superoxide is the primary damaging species. Cysteine blocked this inhibition, suggesting possible involvement of sulfhydryl groups in the inhibition mechanism. Additionally, 1.16 +/- 0.17 mU/g wet wt of xanthine oxidase activity was detected in the postnuclear supernatant of bovine aortic smooth muscle, suggesting the existence of a possible intracellular source of superoxide. This value was calculated to be approximately 5 mU/ml by using a usual value of vascular smooth muscle cellular volume. Thus the level of endogenous xanthine oxidase in vascular smooth muscle is comparable with the level of exogenous xanthine oxidase used in the present study. These findings suggest a potential role of xanthine oxidase-generated superoxide in oxidative damage to vascular smooth muscle during a number of pathophysiological conditions.

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Participation of Reactive Oxygen Intermediates in the Angiotensin II-Activated Signaling Pathways in Vascular Smooth Muscle Cells

Annals of the New York Academy of Sciences ◽

10.1111/j.1749-6632.2000.tb06323.x ◽

2006 ◽

Vol 902 (1) ◽

pp. 283-287 ◽

Cited By ~ 12

Author(s):

TOMOSABURO TAKAHASHI ◽

TAKAHIRO TANIGUCHI ◽

MASANORI OKUDA ◽

AKIHIRO TAKAHASHI ◽

SATORU KAWASAKI ◽

...

Keyword(s):

Smooth Muscle ◽

Angiotensin Ii ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cells ◽

Signaling Pathways ◽

Vascular Smooth Muscle Cells ◽

Reactive Oxygen ◽

Muscle Cells ◽

Reactive Oxygen Intermediates ◽

Oxygen Intermediates

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ACTIVATION OF THE NUCLEAR REGULATORY FACTOR, NF-kappa B, BY REACTIVE OXYGEN INTERMEDIATES (ROI) AND RELEASE OF TNF-alpha FROM CULTURED VASCULAR SMOOTH MUSCLE CELLS

Critical Care Medicine ◽

10.1097/00003246-199801001-00040 ◽

1998 ◽

Vol 26 (Supplement) ◽

pp. 34A

Author(s):

Walter Newman ◽

Debra Warejcka ◽

Manuel Castresana ◽

Kristina Detmer ◽

Martin Dalton ◽

...

Keyword(s):

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cells ◽

Vascular Smooth Muscle Cells ◽

Muscle Cells ◽

Tnf Alpha ◽

Reactive Oxygen Intermediates ◽

Regulatory Factor ◽

Nf Kappa B ◽

Oxygen Intermediates

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Superoxide stimulates IP3-induced Ca2+ release from vascular smooth muscle sarcoplasmic reticulum

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.262.1.h114 ◽

1992 ◽

Vol 262 (1) ◽

pp. H114-H116 ◽

Cited By ~ 13

Author(s):

Y. J. Suzuki ◽

G. D. Ford

Keyword(s):

Smooth Muscle ◽

Sarcoplasmic Reticulum ◽

Vascular Smooth Muscle ◽

Oxygen Toxicity ◽

Cellular Level ◽

Reactive Oxygen Intermediates ◽

Oxygen Intermediates ◽

Sr Protein ◽

Uptake Inhibition ◽

A Site

Reactive oxygen intermediates (ROI) have been implicated in a variety of pathophysiological conditions, and vascular smooth muscle may be a site of damage in such oxygen toxicity. Mechanisms of the effects of these intermediates on vascular smooth muscle at the cellular level, however, have not been well studied. We have previously shown that xanthine oxidase (XO)-generated superoxide radicals (O2-.) inhibited the Ca(2+)-adenosine triphosphatase of vascular smooth muscle sarcoplasmic reticulum (SR) through mechanisms that do not involve H2O2 or hydroxyl radicals. In the present study, we report that the D-myo-inositol 1,4,5-trisphosphate (IP3)-induced Ca2+ release from bovine aortic SR was also affected by O2-(.). Hypoxanthine (100 microM) plus XO (10 mU/ml) in the presence of catalase (100 U/ml) stimulated the IP3-induced Ca2+ release from SR monitored using arsenazo III. At 10 microM IP3, the release was doubled by O2-. treatment. As a consequence of using the higher SR protein concentrations required to observe the Ca2+ release, this effect was independent of Ca2+ uptake inhibition induced by O2-(.). Since the effect of O2-. was not seen when a nonhydrolyzable analogue of IP3 was used to induce Ca2+ release, O-2. may be inhibiting the degradation processes of IP3.

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