Induction of nitric oxide synthase mRNA in coronary  resistance arteries isolated from exercise-trained pigs

Woodman, Christopher R.; Muller, Judy M.; Laughlin, M. Harold; Price, Elmer M.

doi:10.1152/ajpheart.1997.273.6.h2575

Cited by 132 publications

(142 citation statements)

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“…These results are consistent with other studies that have reported elevated NOS mRNA levels in aortas of exercise-trained dogs, and in coronary resistance vessels of exercise-trained pigs (38,39). The expression of inducible NOS and endothelial NOS mRNA was increased in endothelial cells by chronic treadmill training, whereas chronic exercise blunted phenylephrine-induced vascular responses, probably by increasing nitric oxide release via inducible NOS in the rat thoracic aorta (40).…”

Section: Impact Of Different Risk Factors In Combination On the Cardisupporting

confidence: 92%

Vascular adaptive responses to physical exercise and to stress are affected differently by nandrolone administration

Bruder‐Nascimento

Cordellini

2011

Braz J Med Biol Res

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Section: Impact Of Different Risk Factors In Combination On the Cardisupporting

confidence: 92%

Vascular adaptive responses to physical exercise and to stress are affected differently by nandrolone administration

Bruder‐Nascimento

Cordellini

2011

Braz J Med Biol Res

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“…Relative differences in eNOS and SOD-1 mRNA expression in single feed arteries were assessed as described previously (26,28). Briefly, single feed arteries were homogenized in 50 l LiCl lysis buffer by vortexing the sample vigorously for 60 s. The sample was subsequently spun briefly in a microcentrifuge, and the process was repeated four to five times until the artery was completely digested.…”

Section: Quantification Of Enos and Sod-1 Expressionmentioning

confidence: 99%

“…Poly(A) ϩ RNA was isolated from the crude lysate with paramagnetic oligo(dT) beads (Dynal), and first-strand cDNA synthesis was performed in a 20-l volume (Superscript Preamplification System, GIBCO-BRL Life Technologies). Nine microliters of cDNA were used in a PCR using previously published primers and cycling conditions for eNOS or SOD-1 (26,28). The PCR consisted of 25 cycles to ensure that the reaction was within the linear range for the eNOS and SOD-1 primer sets.…”

Section: Quantification Of Enos and Sod-1 Expressionmentioning

confidence: 99%

“…The PCR consisted of 25 cycles to ensure that the reaction was within the linear range for the eNOS and SOD-1 primer sets. All data were standardized by coamplifying eNOS or SOD-1 with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and calculating an eNOS-to-GAPDH or SOD-1-to-GAPDH ratio for each feed artery (26). The sequence for the GAPDH primers has been published previously (28).…”

Section: Quantification Of Enos and Sod-1 Expressionmentioning

confidence: 99%

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Aging induces muscle-specific impairment of endothelium-dependent dilation in skeletal muscle feed arteries

Woodman

Price

Laughlin

2002

Journal of Applied Physiology

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. Aging induces muscle-specific impairment of endothelium-dependent dilation in skeletal muscle feed arteries. J Appl Physiol 93: 1685-1690, 2002; 10.1152/ japplphysiol.00461.2002.-We tested the hypothesis that aging decreases endothelium-dependent vasodilation in feed arteries perfusing rat skeletal muscle. In addition, we tested the hypothesis that attenuated vasodilator responses are associated with decreased endothelial nitric oxide synthase (eNOS) and superoxide dismutase-1 (SOD-1) expression. Soleus feed arteries (SFA) and gastrocnemius feed arteries (GFA) were isolated from young (4 mo) and old (24 mo) male Fischer 344 rats. Feed arteries from the right hindlimb were cannulated with two glass micropipettes for examination of endothelium-dependent [acetylcholine (ACh)] and endothelium-independent [adenosine (Ado) or sodium nitroprusside (SNP)] vasodilator function. Feed arteries from the left hindlimb were frozen and used to assess eNOS and SOD-1 protein and mRNA expression. In SFA, endothelium-dependent dilation to ACh was reduced in old rats (0.9 Ϯ 0.04 vs. 0.8 Ϯ 0.03), whereas dilator responses to Ado and SNP were similar in SFA of young and old rats. In GFA, vasodilator responses to ACh, Ado, and SNP were not altered by age. eNOS and SOD-1 protein expression declined with age in SFA (Ϫ71 and Ϫ54%, respectively) but not in GFA. eNOS and SOD-1 mRNA expression were not altered by age in SFA or GFA. Collectively, these data indicate aging induces muscle-specific impairment of endothelium-dependent vascular function in SFA. endothelial nitric oxide synthase; superoxide dismutase; nitric oxide; acetylcholine; sodium nitroprusside RESULTS FROM SEVERAL STUDIES indicate that endothelial function in conduit arteries declines with age in humans and animals (3,4,7,8,10,11,16,23). The endothelial dysfunction induced by aging is characterized by blunted vasodilator responses of conduit arteries to select endothelium-dependent agonists (3,4,7,8,10,11,16,23). The mechanism(s) for the detrimental effects of age on endothelium-dependent dilation is not fully understood; however, age-associated decrements in the ability of endothelial cells to produce and/or release nitric oxide (NO) may contribute to the dysfunction (3,11,16). This speculation is supported by experimental evidence indicating that vasodilation in response to ACh and bradykinin is impaired in aorta from senescent subjects, whereas dilation to sodium nitroprusside (SNP) is not compromised (3,5,16).An age-associated decline in the expression of endothelial NO synthase (eNOS), decreasing local production of NO, is one mechanism that may contribute to impaired endothelium-mediated dilation in conduit arteries of senescent animals. Indeed, age-related reductions eNOS mRNA expression have been reported in aorta of senescent rats (3, 6). Alternatively, decreased expression of Cu/Zn-dependent superoxide dismutase (SOD-1) may contribute to impaired endothelium-mediated dilation by compromising the ability to scavenge superoxide anion (O 2 Ϫ ⅐), decreasing the bio...

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“…However, this concentration of ¬_NAME has been previously found to act as a muscarinic antagonist (see Buxton et al 1993). Exercise training has been reported to increase eNOS protein in the rat abdominal aorta (4 weeks of treadmill running; Delp & Laughlin, 1997) and in the canine aorta (10 days treadmill running; Sessa et al 1994), and to increase eNOS mRNA in the minipig coronary artery (16 weeks treadmill running, Woodman et al 1997). Therefore, in this present study the larger effect of ¬_NA on the ACh-relaxation of saphenous artery rings from trained animals may result from enhanced levels of NOS protein in this artery.…”

Section: Relaxation Responsesmentioning

confidence: 99%

Exercise Training Enhances Relaxation of the Isolated Guinea‐Pig Saphenous Artery in Response to Acetylcholine

Choate

Kato

Mohan

2000

Experimental Physiology

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The effects of exercise training were investigated on the vascular responses in the isolated guinea‐pig saphenous artery. Exercising animals swam 5 days week‐1 for 6 weeks (60 min day‐1 for weeks 1 and 2; 75 min day‐1 for weeks 3 and 4; 90 min day‐1 for weeks 5 and 6), while control animals were placed into shallow water for the same duration. Trained animals had significantly higher ventricular:body weight ratios, increased citrate synthase activity in the latissimus dorsi, and enhanced Na+ pump concentrations in the latissimus dorsi and gastrocnemius muscles (P < 0.05). In vitro isometric techniques were used to measure constriction and relaxation responses of saphenous artery rings from trained and control animals. There were no significant differences in the constriction responses to KCl (50 mm) and phenylephrine (0.3‐100 μM) in arterial rings from control versus trained animals. Relaxation responses to acetylcholine (10 μM; ACh‐relaxation), following preconstriction with phenylephrine (10 μM), were significantly enhanced in rings from trained animals (P < 0.05). Acetylcholine relaxed the vessels to 47 ± 6% (control) and 18 ± 3% (trained) of the preconstriction responses to phenylephrine. The nitric oxide synthase inhibitor N G‐nitro‐L‐arginine (L‐NA; 50 μM) significantly attenuated the ACh‐relaxation in control and trained animals (P < 0.05). The effect of L‐NA on the ACh‐relaxation was significantly larger in trained (change in ACh‐relaxation with L‐NA = 29 ± 9%) than control (14 ± 3%) animals (P < 0.05). In conclusion, exercise training enhanced the ACh‐relaxation of the isolated guinea‐pig saphenous artery. Inhibition of nitric oxide synthase attenuated the ACh‐relaxation of rings from control and trained animals, but this effect was significantly larger in the vessels from trained animals. These results are consistent with the idea that nitric oxide could contribute to the enhanced ACh‐relaxation of the saphenous artery with exercise training.

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Induction of nitric oxide synthase mRNA in coronary resistance arteries isolated from exercise-trained pigs

Cited by 132 publications

References 11 publications

Vascular adaptive responses to physical exercise and to stress are affected differently by nandrolone administration

Vascular adaptive responses to physical exercise and to stress are affected differently by nandrolone administration

Aging induces muscle-specific impairment of endothelium-dependent dilation in skeletal muscle feed arteries

Exercise Training Enhances Relaxation of the Isolated Guinea‐Pig Saphenous Artery in Response to Acetylcholine

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