Addition of nitric oxide donor S-nitroso-N-acetylcysteine to selective iNOS inhibitor 1400W further improves contractile function in reperfused skeletal muscle

Microsurgery ◽  
2005 ◽  
Vol 25 (4) ◽  
pp. 338-345 ◽  
Author(s):  
Joseph U. Barker ◽  
Wen-Ning Qi ◽  
Yongting Cai ◽  
James R. Urbaniak ◽  
Long-En Chen
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Contractile Function ◽  
Nitric Oxide Donor ◽  
Inos Inhibitor

The effect of the nitric oxide donor sodium nitroprusside on glucose uptake in human primary skeletal muscle cells

Nitric Oxide ◽  
2009 ◽  
Vol 21 (2) ◽  
pp. 126-131 ◽  
Author(s):  
Darren C. Henstridge ◽  
Brian G. Drew ◽  
Melissa F. Formosa ◽  
Alaina K. Natoli ◽  
David Cameron-Smith ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Sodium Nitroprusside ◽  
Glucose Uptake ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Nitric Oxide Donor

Effect of a Nitric Oxide Donor on Microcirculation of Acutely Denervated Skeletal Muscle during Reperfusion

2002 ◽  
Vol 18 (1) ◽  
pp. 053-060 ◽  
Author(s):  
Chen-Hsi Chou ◽  
Long-En Chen ◽  
Anthony V. Seaber ◽  
James R. Urbaniak
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Nitric Oxide Donor

Skeletal muscle contraction-induced vasodilator complement production is dependent on stimulus and contraction frequency

2009 ◽  
Vol 297 (1) ◽  
pp. H433-H442 ◽  
Author(s):  
Ashok K. Dua ◽  
Nickesh Dua ◽  
Coral L. Murrant
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Muscle Fibers ◽  
Nitric Oxide Donor ◽  
Contraction Frequency ◽  
Skeletal Muscle Contraction ◽  
Train Duration ◽  
Arteriolar Vasodilation ◽  
40 Hz

To test the hypothesis that the vasodilator complement that produces arteriolar vasodilation during muscle contraction depends on both stimulus and contraction frequency, we stimulated four to five skeletal muscle fibers in the anesthetized hamster cremaster preparation in situ and measured the change in diameter of arterioles at a site of overlap with the stimulated muscle fibers. Diameter was measured before, during, and after 2 min of skeletal muscle contraction stimulated over a range of stimulus frequencies [4, 20, and 40 Hz; 15 contractions/min (cpm), 250 ms train duration] and a range of contraction frequencies (6, 15, and 60 cpm; 20 Hz stimulus frequency, 250 ms train duration). Muscle fibers were stimulated in the absence and presence of an inhibitor of adenosine receptors [10−6 M xanthine amine congener (XAC)], an ATP-dependent potassium (K+) channel inhibitor (10−5 M glibenclamide), an inhibitor of a source of K+ by inhibition of voltage-dependent K+ channels [3 × 10−4 M 3,4-diaminopyridine (DAP)], and an inhibitor of nitric oxide synthase [10−6 M NG-nitro-l-arginine methyl ester (l-NAME) + 10−7 S-nitroso- N-acetylpenicillamine (a nitric oxide donor)]. l-NAME inhibited the dilations at all stimulus frequencies and contraction frequencies except 60 cpm. XAC inhibited the dilations at all contraction frequencies and stimulus frequencies except 40 Hz. Glibenclamide inhibited all dilations at all stimulus and contraction frequencies, and DAP did not inhibit dilations at any stimulus frequencies while attenuating dilation at a contraction frequency of 60 cpm only. Our data show that the complement of dilators responsible for the vasodilations induced by skeletal muscle contraction differed depending on the stimulus and contraction frequency; therefore, both are important determinants of the dilators involved in the processes of arteriolar vasodilation associated with active hyperemia.

Role of Neuronal Nitric Oxide Synthase in Modulating Microvascular and Contractile Function in Rat Skeletal Muscle

2011 ◽  
Vol 18 (6) ◽  
pp. 501-511 ◽  
Author(s):  
STEVEN W. COPP ◽  
DANIEL M. HIRAI ◽  
SCOTT K. FERGUSON ◽  
TIMOTHY I. MUSCH ◽  
DAVID C. POOLE
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Nitric Oxide Synthase ◽  
Contractile Function ◽  
Neuronal Nitric Oxide Synthase ◽  
Rat Skeletal Muscle ◽  
Oxide Synthase

scholarly journals Effects of neuronal nitric oxide synthase inhibition on microvascular and contractile function in skeletal muscle of aged rats

2012 ◽  
Vol 303 (8) ◽  
pp. H1076-H1084 ◽  
Author(s):  
Daniel M. Hirai ◽  
Steven W. Copp ◽  
Clark T. Holdsworth ◽  
Scott K. Ferguson ◽  
Timothy I. Musch ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Contractile Function ◽  
Muscle Blood Flow ◽  
Force Production ◽  
Microvascular Function ◽  
Brown Norway ◽  
Phosphorescence Quenching ◽  
Nnos Inhibition

Advanced age is associated with derangements in skeletal muscle microvascular function during the transition from rest to contractions. We tested the hypothesis that, contrary to what was reported previously in young rats, selective neuronal nitric oxide (NO) synthase (nNOS) inhibition would result in attenuated or absent alterations in skeletal muscle microvascular oxygenation (Po2mv), which reflects the matching between muscle O2 delivery and utilization, following the onset of contractions in old rats. Spinotrapezius muscle blood flow (radiolabeled microspheres), Po2mv (phosphorescence quenching), O2 utilization (V̇o2; Fick calculation), and submaximal force production were measured at rest and following the onset of contractions in anesthetized old male Fischer 344 × Brown Norway rats (27 to 28 mo) pre- and postselective nNOS inhibition (2.1 μmol/kg S-methyl-l-thiocitrulline; SMTC). At rest, SMTC had no effects on muscle blood flow ( P > 0.05) but reduced V̇o2 by ∼23% ( P < 0.05), which elevated basal Po2mv by ∼18% ( P < 0.05). During contractions, steady-state muscle blood flow, V̇o2, Po2mv, and force production were not altered after SMTC ( P > 0.05 for all). The overall Po2mv dynamics following onset of contractions was also unaffected by SMTC (mean response time: pre, 19.7 ± 1.5; and post, 20.0 ± 2.0 s; P > 0.05). These results indicate that the locus of nNOS-derived NO control in skeletal muscle depends on age and metabolic rate (i.e., rest vs. contractions). Alterations in nNOS-mediated regulation of contracting skeletal muscle microvascular function with aging may contribute to poor exercise capacity in this population.

Effect of Nitric Oxide on the Contractile Function of Rat Reperfused Skeletal Muscle

2002 ◽  
Vol 106 (1) ◽  
pp. 82-85 ◽  
Author(s):  
Kenshiro Ikebe ◽  
Teiji Kato ◽  
Makio Yamaga ◽  
Toru Tsuchida ◽  
Hiroki Irie ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Contractile Function

Reperfusion injury is reduced in skeletal muscle by inhibition of inducible nitric oxide synthase

2003 ◽  
Vol 94 (4) ◽  
pp. 1473-1478 ◽  
Author(s):  
Li Zhang ◽  
Colin G. Looney ◽  
Wen-Ning Qi ◽  
Long-En Chen ◽  
Anthony V. Seaber ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Reperfusion Injury ◽  
Inducible Nitric Oxide Synthase ◽  
Ischemia Reperfusion ◽  
Inos Inhibitor ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

This study evaluated the effects of the selective inducible nitric oxide synthase (iNOS) inhibitor N-[3-(aminomethyl)benzyl]acetamidine (1400W) on the microcirculation in reperfused skeletal muscle. The cremaster muscles from 32 rats underwent 5 h of ischemia followed by 90 min of reperfusion. Rats received either 3 mg/kg 1400W or PBS subcutaneously before reperfusion. We found that blood flow in reperfused muscles was <45% of baseline in controls but sharply recovered to near baseline levels in 1400W-treated animals. There was a significant ( P < 0.01 to P< 0.001) difference between the two groups at each time point throughout the 90 min of reperfusion. Vessel diameters remained <80% of baseline in controls during reperfusion, but recovered to the baseline level in the 1400W group by 20 min, and reached a maximum of 121 ± 14% (mean ± SD) of baseline in 10- to 20-μm arterioles, 121 ± 6% in 21- to 40-μm arterioles, and 115 ± 8% in 41- to 70-μm arteries ( P < 0.01 to P < 0.001). The muscle weight ratio between ischemia-reperfused (left) and non-ischemia-reperfused (right) cremaster muscles was 193 ± 42% of normal in controls and 124 ± 12% in the 1400W group ( P < 0.001). Histology showed that neutrophil extravasation and edema were markedly reduced in 1400W-treated muscles compared with controls. We conclude that ischemia-reperfusion leads to increased generation of NO from iNOS in skeletal muscle and that the selective iNOS inhibitor 1400W reduces the negative effects of ischemia-reperfusion on vessel diameter and muscle blood flow. Thus 1400W may have therapeutic potential in treatment of ischemia-reperfusion injury.

scholarly journals Nitric oxide inhibits calpain-mediated proteolysis of talin in skeletal muscle cells

2000 ◽  
Vol 279 (3) ◽  
pp. C806-C812 ◽  
Author(s):  
Timothy J. Koh ◽  
James G. Tidball
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Sodium Nitroprusside ◽  
Active Site ◽  
Calcium Ionophore ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Nitric Oxide Donor ◽  
Calpain Inhibitor ◽  
Calpain Activity

We tested the hypothesis that nitric oxide can inhibit cytoskeletal breakdown in skeletal muscle cells by inhibiting calpain cleavage of talin. The nitric oxide donor sodium nitroprusside prevented many of the effects of calcium ionophore on C2C12muscle cells, including preventing talin proteolysis and release into the cytosol and reducing loss of vinculin, cell detachment, and loss of cellular protein. These results indicate that nitric oxide inhibition of calpain protected the cells from ionophore-induced proteolysis. Calpain inhibitor I and a cell-permeable calpastatin peptide also protected the cells from proteolysis, confirming that ionophore-induced proteolysis was primarily calpain mediated. The activity of m-calpain in a casein zymogram was inhibited by sodium nitroprusside, and this inhibition was reversed by dithiothreitol. Previous incubation with the active site-targeted calpain inhibitor I prevented most of the sodium nitroprusside-induced inhibition of m-calpain activity. These data suggest that nitric oxide inhibited m-calpain activity via S-nitrosylation of the active site cysteine. The results of this study indicate that nitric oxide produced endogenously by skeletal muscle and other cell types has the potential to inhibit m-calpain activity and cytoskeletal proteolysis.

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