SOD-1 expression in pig coronary arterioles is increased by exercise training.

Coronary arterioles of exercise-trained (EX) pigs have enhanced nitric oxide (NO.)-dependent dilation. Evidence suggests that the biological half-life of NO. depends in part on the management of the superoxide anion. The purpose of this study was to test the hypothesis that expression of cytosolic copper/zinc-dependent superoxide dismutase (SOD)-1 is increased in coronary arterioles as a result of exercise training. Male Yucatan pigs either remained sedentary (SED, n = 4) or were EX (n = 4) on a motorized treadmill for 16-20 wk. Individual coronary arterioles ( approximately 100-microm unpressurized internal diameter) were dissected and frozen. Coronary arteriole SOD-1 protein (via immunoblots) increased as a result of exercise training (2.16 +/- 0.35 times SED levels) as did SOD-1 enzyme activity (measured via inhibition of pyrogallol autooxidation; approximately 75% increase vs. SED). In addition, SOD-1 mRNA levels (measured via RT-PCR) were higher in EX arterioles (1.68 +/- 0.16 times the SED levels). There were no effects of exercise training on the levels of SOD-2 (mitochondrial), catalase, or p67(phox) proteins. Thus chronic aerobic exercise training selectively increases the levels of SOD-1 mRNA, protein, and enzymatic activity in porcine coronary arterioles. Increased SOD-1 could contribute to the enhanced NO.-dependent dilation previously observed in EX porcine coronary arterioles by improving management of superoxide in the vascular cell environment, thus prolonging the biological half-life of NO.

[1]  G. Schuler,et al.  Effect of Exercise on Coronary Endothelial Function in Patients With Coronary Artery Disease , 2000 .

[2]  G. Kajiyama,et al.  Regular aerobic exercise augments endothelium-dependent vascular relaxation in normotensive as well as hypertensive subjects: role of endothelium-derived nitric oxide. , 1999, Circulation.

[3]  P. de Coppet,et al.  The Human Copper-Zinc Superoxide Dismutase Gene (SOD1) Proximal Promoter Is Regulated by Sp1, Egr-1, and WT1 via Non-canonical Binding Sites* , 1999, The Journal of Biological Chemistry.

[4]  B. Davidson,et al.  Superoxide production in vascular smooth muscle contributes to oxidative stress and impaired relaxation in atherosclerosis. , 1998, Circulation research.

[5]  StefanoTaddei,et al.  Vitamin C Improves Endothelium-Dependent Vasodilation by Restoring Nitric Oxide Activity in Essential Hypertension , 1998 .

[6]  R. Busse,et al.  Pulsatile Stretch and Shear Stress: Physical Stimuli Determining the Production of Endothelium-Derived Relaxing Factors , 1998, Journal of Vascular Research.

[7]  K. H. Park,et al.  Transcriptional activation of the Cu,Zn-superoxide dismutase gene through the AP2 site by ginsenoside Rb2 extracted from a medicinal plant, Panax ginseng. , 1996, The Journal of biological chemistry.

[8]  V. Huxley,et al.  Endothelium-Mediated Control of the Coronary Circulation , 1996 .

[9]  R M Nerem,et al.  Shear stress modulates expression of Cu/Zn superoxide dismutase in human aortic endothelial cells. , 1996, Circulation research.

[10]  D. Harrison,et al.  Angiotensin II-mediated hypertension in the rat increases vascular superoxide production via membrane NADH/NADPH oxidase activation. Contribution to alterations of vasomotor tone. , 1996, The Journal of clinical investigation.

[11]  S. Marklund,et al.  The interstitium of the human arterial wall contains very large amounts of extracellular superoxide dismutase. , 1995, Arteriosclerosis, thrombosis, and vascular biology.

[12]  B. Halliwell,et al.  Nitric oxide and oxygen radicals: a question of balance , 1995, FEBS letters.

[13]  S. Diamond,et al.  Constitutive NOS expression in cultured endothelial cells is elevated by fluid shear stress. , 1995, The American journal of physiology.

[14]  C. Jones,et al.  Regulation of coronary blood flow: coordination of heterogeneous control mechanisms in vascular microdomains. , 1995, Cardiovascular research.

[15]  M. Wolin,et al.  Sites of superoxide anion production detected by lucigenin in calf pulmonary artery smooth muscle. , 1994, The American journal of physiology.

[16]  M. Laughlin,et al.  Exercise training-induced increase in coronary transport capacity. , 1994, Medicine & Science in Sports & Exercise.

[17]  N. Cable,et al.  Modification of forearm resistance vessels by exercise training in young men. , 1994, Journal of applied physiology.

[18]  J. Qiao,et al.  Genetic evidence for a common pathway mediating oxidative stress, inflammatory gene induction, and aortic fatty streak formation in mice. , 1994, The Journal of clinical investigation.

[19]  H. T. Kim,et al.  Study of 5'-flanking region of human Cu/Zn superoxide dismutase. , 1994, Biochemical and biophysical research communications.

[20]  P. Kaminski,et al.  NADH oxidoreductase is a major source of superoxide anion in bovine coronary artery endothelium. , 1994, The American journal of physiology.

[21]  M. Laughlin,et al.  Vasodilator responses of coronary resistance arteries of exercise-trained pigs. , 1994, Circulation.

[22]  K. Pritchard,et al.  Chronic exercise in dogs increases coronary vascular nitric oxide production and endothelial cell nitric oxide synthase gene expression. , 1994, Circulation research.

[23]  T. Hintze,et al.  Chronic exercise enhances endothelium-mediated dilation of epicardial coronary artery in conscious dogs. , 1993, Circulation research.

[24]  H. Alessio.  Exercise-induced oxidative stress. , 1993, Medicine and science in sports and exercise.

[25]  H. Adams,et al.  Effects of exercise training on vasomotor reactivity of porcine coronary arteries. , 1992, The American journal of physiology.

[26]  I. Piña,et al.  Statement on exercise. Benefits and recommendations for physical activity programs for all Americans. A statement for health professionals by the Committee on Exercise and Cardiac Rehabilitation of the Council on Clinical Cardiology, American Heart association. , 1992, Circulation.

[27]  B. Venkaiah,et al.  Characterization of superoxide dismutase from south Indian scorpion venom. , 1992, Biochemistry International.

[28]  D. Harrison,et al.  Chronic treatment with polyethylene-glycolated superoxide dismutase partially restores endothelium-dependent vascular relaxations in cholesterol-fed rabbits. , 1991, Circulation research.

[29]  M. Wolin,et al.  Inhibition of coronary artery superoxide dismutase attenuates endothelium-dependent and -independent nitrovasodilator relaxation. , 1991, Circulation research.

[30]  D. Harrison,et al.  Release of intact endothelium-derived relaxing factor depends on endothelial superoxide dismutase activity. , 1991, The American journal of physiology.

[31]  M. Laughlin,et al.  Exercise training increases coronary transport reserve in miniature swine. , 1989, Journal of applied physiology.

[32]  S. Moncada,et al.  Synthesis of nitric oxide from L-arginine by neutrophils. Release and interaction with superoxide anion. , 1989, The Biochemical journal.

[33]  Z. Katušić,et al.  Superoxide anion is an endothelium-derived contracting factor. , 1989, The American journal of physiology.

[34]  D. Stewart,et al.  Free radicals inhibit endothelium-dependent dilation in the coronary resistance bed. , 1988, The American journal of physiology.

[35]  L. Ignarro,et al.  Endothelium-derived relaxing factor produced and released from artery and vein is nitric oxide. , 1987, Proceedings of the National Academy of Sciences of the United States of America.

[36]  M. Laughlin,et al.  Myocardial capillarity and maximal capillary diffusion capacity in exercise-trained dogs. , 1987, Journal of applied physiology.

[37]  S. Moncada,et al.  Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor , 1987, Nature.

[38]  George I. Bell,et al.  cDNA sequence coding for human kidney catalase , 1986, Nucleic Acids Res..

[39]  S. Moncada,et al.  Superoxide anion is involved in the breakdown of endothelium-derived vascular relaxing factor , 1986, Nature.

[40]  M. Laughlin.  Effects of exercise training on coronary transport capacity. , 1985, Journal of applied physiology.

[41]  Y. Groner,et al.  Nucleotide sequence and expression of human chromosome 21-encoded superoxide dismutase mRNA. , 1983, Proceedings of the National Academy of Sciences of the United States of America.

[42]  G. Brooks,et al.  Free radicals and tissue damage produced by exercise. , 1982, Biochemical and biophysical research communications.

[43]  Y. Wang,et al.  MYOCARDIAL BLOOD FLOW AND OXYGEN CONSUMPTION DURING EXERCISE , 1977, Annals of the New York Academy of Sciences.

[44]  S. Marklund,et al.  Involvement of the superoxide anion radical in the autoxidation of pyrogallol and a convenient assay for superoxide dismutase. , 1974, European journal of biochemistry.

[45]  C. Tipton,et al.  A submaximal test for dogs: evaluation of effects of training, detraining, and cage confinement. , 1974, Journal of applied physiology.

[46]  D. E. Gregg,et al.  Effect of Exercise on Cardiac Output, Left Coronary Flow and Myocardial Metabolism in the Unanesthetized Dog , 1965, Circulation research.

[47]  M. Laughlin,et al.  Flow regulation of ecNOS and Cu/Zn SOD mRNA expression in porcine coronary arterioles. , 1999, The American journal of physiology.

[48]  E. Price,et al.  Induction of nitric oxide synthase mRNA in coronary resistance arteries isolated from exercise-trained pigs. , 1997, American journal of physiology. Heart and circulatory physiology.