20-HETE Contributes to Myogenic Activation of Skeletal Muscle Resistance Arteries in Brown Norway and Sprague–Dawley Rats

Although arterial dilator reactivity is severely impaired during exposure of animals to chronic intermittent hypoxia (CIH), few studies have characterized vasoconstrictor responsiveness in resistance arteries of this model of sleep-disordered breathing. Sprague-Dawley rats were exposed to CIH (10% inspired O2 fraction for 1 min at 4-min intervals; 12 h/day) for 14 days. Control rats were housed under normoxic conditions. Diameters of isolated gracilis muscle resistance arteries (GA; 120–150 μm) were measured by television microscopy before and during exposure to norepinephrine (NE) and angiotensin II (ANG II) and at various intraluminal pressures between 20 and 140 mmHg in normal and Ca2+-free physiological salt solution. There was no difference in the ability of GA to constrict in response to ANG II ( P = 0.42; not significant; 10−10–10−7 M). However, resting tone, myogenic activation, and vasoconstrictor responses to NE ( P < 0.001; 10−9–10−6 M) were reduced in CIH vs. controls. Treatment of rats with the superoxide scavenger 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (tempol; 1 mM) in the drinking water restored myogenic responses and NE-induced constrictions of CIH rats, suggesting that elevated superoxide production during exposure to CIH attenuates vasoconstrictor responsiveness to NE and myogenic activation in skeletal muscle resistance arteries. CIH also leads to an increased stiffness and reduced vessel wall distensibility that were not correctable with oral tempol treatment.

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High-salt diet impairs hypoxia-induced cAMP production and hyperpolarization in rat skeletal muscle arteries

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2001.281.4.h1808 ◽

2001 ◽

Vol 281 (4) ◽

pp. H1808-H1815 ◽

Cited By ~ 23

Author(s):

Jefferson C. Frisbee ◽

Francis A. Sylvester ◽

Julian H. Lombard

Keyword(s):

Skeletal Muscle ◽

Cholera Toxin ◽

High Salt ◽

Sprague Dawley ◽

Resistance Arteries ◽

High Salt Diet ◽

Sprague Dawley Rats ◽

Prostaglandin H ◽

Camp Levels

This study determined the effects of hypoxia on diameter, vascular smooth muscle (VSM) transmembrane potential ( E m), and vascular cAMP levels for in vitro cannulated skeletal muscle resistance arteries (gracilis arteries) from Sprague-Dawley rats fed a low-salt (LS) or a high-salt (HS) diet. Arterial diameter and VSM E m were measured in response to hypoxia, iloprost, cholera toxin, forskolin, and aprikalim. In HS rats, arterial dilation and VSM hyperpolarization after hypoxia, iloprost, and cholera toxin were impaired versus responses in LS rats, whereas responses to forskolin and aprikalim were unaltered. Blockade of prostaglandin H2 and thromboxane A2 receptors had no effect on responses to hypoxia or iloprost in vessels from both rat groups, suggesting that inappropriate activation of these receptors does not contribute to the impaired hypoxic dilation with HS. Hypoxia, cholera toxin, and iloprost increased vascular cAMP levels in vessels of LS rats only, whereas forskolin increased cAMP levels in all vessels. These data suggest that reduced hypoxic dilation of skeletal muscle microvessels in rats on a HS diet may reflect an impaired ability of VSM to produce cAMP after exposure to prostacyclin.

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Effects of Exercise Intensity on PGC-1α, PPAR-γ, and Insulin Resistance in Skeletal Muscle of High Fat Diet-fed Sprague-Dawley Rats

Journal of the Korean Society of Food Science and Nutrition ◽

10.3746/jkfn.2014.43.7.963 ◽

2014 ◽

Vol 43 (7) ◽

pp. 963-971

Author(s):

Hyun-Lyung Jung ◽

Ho-Youl Kang

Keyword(s):

Insulin Resistance ◽

Skeletal Muscle ◽

Exercise Intensity ◽

High Fat Diet ◽

Sprague Dawley ◽

High Fat ◽

Ppar Γ ◽

Sprague Dawley Rats

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Effects of Endurance Exercise and High-Fat Diet on Insulin Resistance and Ceramide Contents of Skeletal Muscle in Sprague-Dawley Rats

Korean Diabetes Journal ◽

10.4093/kdj.2010.34.4.244 ◽

2010 ◽

Vol 34 (4) ◽

pp. 244 ◽

Cited By ~ 9

Author(s):

Hyun Lyung Jung ◽

Ho Youl Kang

Keyword(s):

Insulin Resistance ◽

Skeletal Muscle ◽

Endurance Exercise ◽

High Fat Diet ◽

Sprague Dawley ◽

High Fat ◽

Sprague Dawley Rats

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Effect of low-potassium diet on rat exercise hyperthermia and heatstroke mortality

Journal of Applied Physiology ◽

10.1152/jappl.1981.51.1.8 ◽

1981 ◽

Vol 51 (1) ◽

pp. 8-13 ◽

Cited By ~ 13

Author(s):

R. W. Hubbard ◽

M. Mager ◽

W. D. Bowers ◽

I. Leav ◽

G. Angoff ◽

...

Keyword(s):

Skeletal Muscle ◽

Body Weight ◽

Plasma Potassium ◽

Heat Illness ◽

Sprague Dawley ◽

Heat Gain ◽

Sprague Dawley Rats ◽

Low Potassium ◽

Work Done ◽

Low K

A total of 182 male Sprague-Dawley rats weighing 250–300 g were fed either a control (n = 122) diet for 32 days. The diets contained either 125 or 8 meq potassium/kg, respectively. Rats fed the low-K diet gained weight at only one-third the rate of controls (1.7 vs. 5.2 g/day), and their skeletal muscle and plasma potassium levels were reduced by 28 and 47%, respectively. When run to exhaustion at either 15 or 20 degrees C, low K+-fed rats accomplished less than one-half of the work done by the controls (26 vs. 53 kg. m) but exhibited a markedly greater rate of heat gain per kilogram-meter of work than controls (0.12 vs. 0.05 degrees C)ambient temperature of 20 degrees C, the rats of the low-K+ group despite large differences in body weight (-25%), run time temperature and twice (33 vs 17%) the mortality rate of the controls. Postexercise increases in circulating potassium (less than 90%) of heat-injured rats raised the plasma levels of low K+-fed rats to normal (5.9 +/- 2.2 meq/l). These results appear to characterize the existence of an insidious and, therefore, undocumented form of fatal exertion-induced heat illness.

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Mammalian target of rapamycin pathway is up-regulated by both acute endurance exercise and chronic muscle contraction in rat skeletal muscle

Applied Physiology Nutrition and Metabolism ◽

10.1139/apnm-2012-0405 ◽

2013 ◽

Vol 38 (8) ◽

pp. 862-869 ◽

Cited By ~ 15

Author(s):

Brittany A. Edgett ◽

Melanie L. Fortner ◽

Arend Bonen ◽

Brendon J. Gurd

Keyword(s):

Skeletal Muscle ◽

Endurance Exercise ◽

Gastrocnemius Muscle ◽

Contractile Activity ◽

Mammalian Target Of Rapamycin ◽

Mtor Pathway ◽

Initiation Factor ◽

Eukaryotic Initiation Factor ◽

Sprague Dawley ◽

Sprague Dawley Rats

This study examined changes in the expression of translation initiation regulatory proteins and mRNA following both an acute bout of endurance exercise and chronic muscle contractile activity. Female Sprague Dawley rats ran for 2 h at 15 m·min−1 followed by an increase in speed of 5 m·min−1 every 5 min until volitional fatigue. The red gastrocnemius muscle was harvested from nonexercised animals (control; n = 6) and from animals that exercised either immediately after exercise (n = 6) or following 3 h of recovery from exercise (n = 6). Compared with control, ribosomal protein S6 (rpS6) mRNA was elevated (p < 0.05) at both 0 h (+32%) and 3 h (+47%). Both a catalytic subunit of eukaryotic initiation factor 2B (eIF2Bε) (+127%) and mammalian target of rapamycin (mTOR) mRNA (+44%) were increased at 3 h, compared with control. Phosphorylation of mTOR (+40%) and S6 kinase 1 (S6K1) (+266%) were increased immediately after exercise (p < 0.05). Female Sprague Dawley rats also underwent chronic stimulation of the peroneal nerve continuously for 7 days. The red gastrocnemius muscle was removed 24 h after cessation of the stimulation. Chronic muscle stimulation increased (p < 0.05) mTOR protein (+74%), rpS6 (+31%), and eukaryotic initiation factor 2α (+44%, p = 0.069), and this was accompanied by an increase in cytochrome c (+31%). Increased resting phosphorylation was observed for rpS6 (+51%) (p < 0.05) but not for mTOR or eukaryotic initiation factor 4E binding protein 1. These experiments demonstrate that both acute and chronic contractile activity up-regulate the mTOR pathway and mitochondrial content in murine skeletal muscle. This up-regulation of the mTOR pathway may increase translation efficiency and may also represent an important control point in exercise-mediated mitochondrial biogenesis.

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In vivo leucine oxidation at rest and during two intensities of exercise

Journal of Applied Physiology ◽

10.1152/jappl.1982.53.4.947 ◽

1982 ◽

Vol 53 (4) ◽

pp. 947-954 ◽

Cited By ~ 28

Author(s):

P. W. Lemon ◽

F. J. Nagle ◽

J. P. Mullin ◽

N. J. Benevenga

Keyword(s):

Skeletal Muscle ◽

Specific Activity ◽

Muscle Metabolism ◽

Weighted Average ◽

Mixed Diet ◽

Sprague Dawley ◽

Tracer Dose ◽

Sprague Dawley Rats ◽

14Co2 Production

After ingestion of a mixed diet containing a tracer dose (10 muCi) of L-[1–14C]leucine (Leu), 32 male Sprague-Dawley rats (70–90 g) remained at rest (R) or completed 1 h exercise at 80 (E80) or 40% VO2max (E40). 14CO2 production was assessed for 6 h (exercise occurred from h 2 to 3). Four rats were killed at 2, 3, 4, and 6 h (R), at 3 and 6 h (E80), and at 6 h (E40). Determinations were 1) tissue specific activity dpm X mumol-1 from a) mixed skeletal muscle (gastrocnemius, soleus, quadriceps, and hamstrings) and b) liver and 2) radioactivity remaining in the gastrointestinal tract (GIT). Leu oxidized (mumol) was estimated (14 CO2 dpm X tissue sp act dpm-1 X mumol-1) independently from skeletal muscle and liver. Results were 1) 14CO2 production increased in both E80 and E40 compared with R (P less than 0.05), 2) E80 14CO2 increase was greater than E40 (P less than 0.05), 3) GIT absorption was reduced in E80 and E40 compared with R (P less than 0.05), and 4) exercise Leu oxidation (weighted average of tissue estimates) was 26% greater than R (P less than 0.05). The origin and site of the increased Leu oxidation cannot be determined from the present data; however, due to the magnitude of increase in skeletal muscle metabolism relative to other tissues during exercise, it is probable that skeletal muscle plays a significant role.

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Both peripheral chylomicron catabolism and hepatic uptake of remnants are defective in nephrosis

AJP Renal Physiology ◽

10.1152/ajprenal.1992.263.2.f335 ◽

1992 ◽

Vol 263 (2) ◽

pp. F335-F341

Author(s):

G. A. Kaysen ◽

L. Mehendru ◽

X. M. Pan ◽

I. Staprans

Keyword(s):

Skeletal Muscle ◽

Nephrotic Syndrome ◽

Potential Risk ◽

Vascular Endothelium ◽

Hepatic Uptake ◽

Absolute Rate ◽

Sprague Dawley ◽

Primary Defect ◽

Heymann Nephritis ◽

Sprague Dawley Rats

We showed previously that proteinuria caused delayed chylomicron (CM) clearance in the rat and postulated the existence of a primary defect in CM hydrolysis. It was possible that reduced CM clearance resulted from increased lipogenesis causing saturation of catabolic sites and not from a primary defect in CM catabolism. To clarify this point we measured kinetically the absolute rate of triglyceride (TG) uptake from CM in rats with Heymann nephritis (HN) and normal Sprague-Dawley rats (SD) and determined TG uptake in individual tissues using [3H]TG- and [14C]cholesterol-labeled CM. Hepatic [14C]cholesterol uptake was reduced in HN (69.3 +/- 6 vs. 7.2 +/- 2% of dose, P less than 0.001). TG uptake was reduced in HN measured kinetically (1.01 +/- 0.09 vs. 0.213 +/- 0.028 mg TG.min-1.100 g body wt-1, P less than 0.001) and reduced in all tissues (heart, skeletal muscle, fat, and liver). CM are catabolized on the vascular endothelium to atherogenic, cholesterol-rich remnant (CM remnant) particles, which are then rapidly taken up by the liver. We measured hepatic CM remnant uptake in SD and in HN using [14C]cholesterol-labeled CM remnant. CM remnant uptake was significantly reduced in HN (58 +/- 1.2 vs. 20 +/- 0.86% uptake, P less than 0.01). CM remnants were increased significantly in plasma of HN. Thus the nephrotic syndrome causes a primary defect in the uptake of TG from CM that is expressed in all tissues and a separate defect in hepatic CM remnant uptake. Although CM remnant generation is impaired because of defective CM hydrolysis, the defect in hepatic CM remnant uptake is so severe that these particles accumulate in blood, posing a potential risk for atherogenesis.

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Hindlimb unweighting alters endothelium-dependent vasodilation and ecNOS expression in soleus arterioles

Journal of Applied Physiology ◽

10.1152/jappl.2000.89.4.1483 ◽

2000 ◽

Vol 89 (4) ◽

pp. 1483-1490 ◽

Cited By ~ 36

Author(s):

William G. Schrage ◽

Christopher R. Woodman ◽

M. Harold Laughlin

Keyword(s):

Sodium Nitroprusside ◽

Group Treatment ◽

Day Treatment ◽

Weight Bearing ◽

Immunoblot Analysis ◽

Sprague Dawley ◽

Resistance Arteries ◽

Protein Levels ◽

Sprague Dawley Rats ◽

Mrna And Protein Expression

The purpose of this study was to test the hypothesis that endothelium-dependent dilation is impaired in soleus resistance arteries from hindlimb-unweighted (HLU) rats. Male Sprague-Dawley rats (300–350 g) were exposed to HLU ( n = 14) or weight-bearing control (Con, n = 14) conditions for 14 days. After the 14-day treatment period, soleus first-order (1A) arterioles were isolated and cannulated with micropipettes to assess vasodilator responses to an endothelium-dependent dilator, ACh (10−9–10−4 M), and an endothelium-independent dilator, sodium nitroprusside (SNP, 10−9–10−4 M). Arterioles from HLU rats were smaller than Con arterioles (maximal passive diameter = 140 ± 4 and 121 ± 4 μm in Con and HLU, respectively) but developed similar spontaneous myogenic tone (43 ± 3 and 45 ± 3% in Con and HLU, respectively). Arteries from Con and HLU rats dilated in response to increasing doses of ACh, but dilation was impaired in arterioles from HLU rats ( P = 0.03), as was maximal dilation to ACh (85 ± 4 and 65 ± 4% possible dilation in Con and HLU, respectively). Inhibition of nitric oxide (NO) synthase (NOS) with N ω-nitro-l-arginine (300 μM) reduced ACh dilation by ∼40% in arterioles from Con rats and eliminated dilation in arterioles from HLU rats. The cyclooxygenase inhibitor indomethacin (50 μM) did not significantly alter dilation to ACh in either group. Treatment with N ω-nitro-l-arginine + indomethacin eliminated all ACh dilation in Con and HLU rats. Dilation to sodium nitroprusside was not different between groups ( P = 0.98). To determine whether HLU decreased expression of endothelial cell NOS (ecNOS), mRNA and protein levels were measured in single arterioles with RT-PCR and immunoblot analysis. The ecNOS mRNA and protein expression was significantly lower in arterioles from HLU rats than in Con arterioles (20 and 65%, respectively). Collectively, these data indicate that HLU impairs ACh dilation in soleus 1A arterioles, in part because of alterations in the NO pathway.

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