Nitric oxide release is present from incubated skeletal muscle preparations

Balon, Thomas W.; Nadler, Jerry L.

doi:10.1152/jappl.1994.77.6.2519

Cited by 368 publications

(312 citation statements)

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“…Prior contraction of isolated incubated skeletal muscle preparations causes an increased rate of NO release [15,16]. Recent studies in itro with NO donors have provided evidence that this gaseous signalling molecule stimulates glucose transport, glycolysis and glucose oxidation in skeletal muscle [8].…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies in itro with NO donors have provided evidence that this gaseous signalling molecule stimulates glucose transport, glycolysis and glucose oxidation in skeletal muscle [8]. Inhibition of NOS, which forms NO, decreases basal glucose transport in itro [15] and causes insulin resistance in i o [26], although this latter effect is disputed [27]. NO activates the soluble form of guanylate cyclase [11].…”

Section: Discussionmentioning

confidence: 99%

“…Because the rate of release of NO is increased by prior contraction of skeletal muscle [15,16] and NO stimulates glucose utilization [8], it is important to measure the activity of the NO\cGMP system in insulin-resistant muscle. In addition, the expression of NOS increases in skeletal muscles isolated from exercise-trained rats [17].…”

Section: Introductionmentioning

confidence: 99%

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Evidence for altered sensitivity of the nitric oxide/cGMP signalling cascade in insulin-resistant skeletal muscle

Young

Leighton

1998

Biochemical Journal

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Nitric oxide activates guanylate cyclase to form cGMP, comprising a signalling system that is believed to be a distinct mechanism for increasing glucose transport and metabolism in skeletal muscle. The effects of a selective cGMP phosphodiesterase inhibitor, zaprinast, on basal glucose utilization was investigated in incubated rat soleus muscle preparations isolated from both insulin-sensitive (lean Zucker; Fa/?) and insulin-resistant (obese Zucker; fa/fa) rats. Zaprinast at 27 μM significantly increased cGMP levels in incubated soleus muscle isolated from lean, but not obese, Zucker rats. Muscles were incubated with 14C-labelled glucose and various concentrations of zaprinast (3, 27 and 243 μM). Zaprinast (at 27 and 243 μM) significantly increased rates of net and 14C-labelled lactate release and of glycogen synthesis in lean Zucker rat soleus muscle; glucose oxidation was also increased by 27 μM zaprinast. In addition, regardless of concentration, the phosphodiesterase inhibitor failed to increase any aspect of 14C-labelled glucose utilization in soleus muscles isolated from obese Zucker rats. The maximal activity of nitric oxide synthase (NOS) was significantly decreased in insulin-resistant obese Zucker muscles. Thus the lack of effect of zaprinast in insulin-resistant skeletal muscle is consistent with decreased NOS activity. To test whether there is a defect in insulin-resistant skeletal muscle for endogenous activation of guanylate cyclase, soleus muscles were isolated from both insulin-sensitive and insulin-resistant Zucker rats and incubated with various concentrations of the NO donor sodium nitroprusside (SNP; 0.1, 1, 5 and 15 mM). SNP significantly increased rates of net and 14C-labelled lactate release, as well as glucose oxidation in muscles isolated from both insulin-sensitive and insulin-resistant rats. A decreased response to SNP was observed in the dose-dependent generation of cGMP within isolated soleus muscles from insulin-resistant rats. A possible link between impaired NO/cGMP signalling and abnormal glucose utilization by skeletal muscle is discussed.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Evidence for altered sensitivity of the nitric oxide/cGMP signalling cascade in insulin-resistant skeletal muscle

Young

Leighton

1998

Biochemical Journal

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“…Electrical stimulation, eliciting muscle contraction causes release of NO [15]. Animal studies have demonstrated that NO donor drugs such as sodium nitroprusside (SNP) increase glucose transport in skeletal muscle [13,[16][17][18][19].…”

Section: Introductionmentioning

confidence: 99%

Effects of the nitric oxide donor, sodium nitroprusside, on resting leg glucose uptake in patients with type 2 diabetes

et al. 2005

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Aims/hypothesis: Nitric oxide (NO) has been implicated as an important signalling molecule in the contraction-mediated glucose uptake pathway and may represent a novel strategy for blood glucose control. The current study sought to determine whether acute infusion of the NO donor, sodium nitroprusside (SNP), increases leg glucose uptake at rest in patients with type 2 diabetes. Methods: Fifteen male patients with type 2 diabetes (aged 54±4 years, mean±SD) were entered into a randomised, cross-over design study, examining the effect of a 30-min intra-femoral infusion of SNP on leg glucose uptake. Comparison was made with a 30-min infusion of verapamil, titrated to elicit similar leg blood flow responses to SNP. Leg blood flow was measured by thermodilution in the femoral vein, and leg glucose uptake was calculated as the product of leg blood flow and the femoral arterio-venous (A-V) glucose concentration gradient. Results: The two drugs increased leg blood flow to a similar extent (p= 0.50). Both leg A-V glucose concentration gradient (SNP 0.12±0.05, verapamil −0.06±0.04 mmol/l; mean±SEM, p=0.03) and leg glucose uptake (SNP 0.17±0.09, verapamil −0.09±0.06 mmol/min; p=0.03) were higher with the SNP treatment than with verapamil. These results occurred independently of any significant difference in plasma insulin concentration between drugs (p=0.56). Conclusions/interpretation: Acute infusion of SNP resulted in greater glucose uptake relative to verapamil. NO may therefore be an important mediator of peripheral glucose disposal and a potential therapeutic target in patients with type 2 diabetes.

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“…Nitric oxide (NO), generated by nNOS in muscle fibres (Balon & Nadler 1994) or eNOS in blood vessel endothelium in response to an increased shear stress (Fleming & Busse 2003), contributes to the hyperaemia observed during acute muscle contractions in animals (Hirai et al . 1994) and humans (Boushel 2003, Schrage et al .…”

Section: Discussionmentioning

confidence: 99%

Shear stress‐induced angiogenesis in mouse muscle is independent of the vasodilator mechanism and quickly reversible

et al. 2016

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AimIs modulation of skeletal muscle capillary supply by altering blood flow due to a presumptive shear stress response per se, or dependent on the vasodilator mechanism?MethodsThe response to four different vasodilators, and cotreatment with blockers of NO and prostaglandin synthesis, was compared. Femoral artery blood flow was correlated with capillary‐to‐fibre ratio (C:F) and protein levels of putative angiogenic compounds.ResultsAll vasodilators induced a similar increase in blood flow after 14 days, with a similar effect on C:F (1.62 ± 0.05, 1.60 ± 0.01, 1.57 ± 0.06, 1.57 ± 0.07, respectively, all P < 0.05 vs. control 1.20 ± 0.01). Concomitant inhibitors revealed differential effects on blood flow and angiogenesis, demonstrating that a similar response may have different signalling origins. The time course of this response with the most commonly used vasodilator, prazosin, showed that blood flow increased from 0.40 mL min−1 to 0.61 mL min−1 by 28 days (P < 0.05), dropped within 1 week after the cessation of treatment (0.54 mL min−1; P < 0.05) and returned to control levels by 6 weeks. In parallel with FBF, capillary rarefaction began within 1 week (P < 0.05), giving C:F values similar to control by 2 weeks. Of the dominant signalling pathways, prazosin decreased muscle VEGF, but increased its cognate receptor Flk‐1 (both P < 0.01); levels of eNOS varied with blood flow (P < 0.05), and Ang‐1 initially increased, while its receptor Tie‐2 was unchanged, with only modest changes in the antiangiogenic factor TSP‐1.ConclusionHyperaemia‐induced angiogenesis, likely in response to elevated shear stress, is independent of the vasodilator involved, with a rapid induction and quick regression following the stimulus withdrawal.

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Nitric oxide release is present from incubated skeletal muscle preparations

Cited by 368 publications

References 0 publications

Evidence for altered sensitivity of the nitric oxide/cGMP signalling cascade in insulin-resistant skeletal muscle

Evidence for altered sensitivity of the nitric oxide/cGMP signalling cascade in insulin-resistant skeletal muscle

Effects of the nitric oxide donor, sodium nitroprusside, on resting leg glucose uptake in patients with type 2 diabetes

Shear stress‐induced angiogenesis in mouse muscle is independent of the vasodilator mechanism and quickly reversible

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