scholarly journals Autoradiographic visualization of beta-adrenergic receptors in normal and denervated skeletal muscle.

1979 ◽  
Vol 27 (10) ◽  
pp. 1308-1311 ◽  
Author(s):  
B Lavenstein ◽  
W K Engel ◽  
N B Reddy ◽  
S Carroll
Keyword(s):  
Skeletal Muscle ◽  
Blood Vessels ◽  
Adrenergic Receptors ◽  
Cellular Localization ◽  
Muscle Fibers ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Adrenergic Blocker

Autoradiographic localization of beta-adrenergic receptors in rat skeletal muscle in vivo was achieved utilizing [125I]-iodohydroxybenzylpindolol, a potent beta-adrenergic blocker with high affinity and specificity for those receptors. In normal muscle the beta-adrenergic receptors were localized mainly to blood vessels, arterioles greater than venules, with much less concentration of grains over the fascicles of muscle fibers. One week after denervation there was an increase in binding both to blood vessels and muscle fibers, more so in soleus and gactrocnemius than in extensor digitorum longus. While these results parallel in vitro biochemical studies, they dictate caution when inferring cellular localization of beta-adrenergic receptors (and other molecules) solely on the basis of biochemical techniques applied to subcellular fractions of whole-organ homogenates.

Skeletal muscle beta-adrenergic receptors: variations due to fiber type and training

1984 ◽  
Vol 246 (2) ◽  
pp. E160-E167 ◽  
Author(s):  
R. S. Williams ◽  
M. G. Caron ◽  
K. Daniel
Keyword(s):  
Skeletal Muscle ◽  
Adrenergic Receptors ◽  
Fiber Type ◽  
Succinic Dehydrogenase ◽  
Oxidative Capacity ◽  
Treadmill Running ◽  
Beta Adrenergic Receptors ◽  
Control Groups ◽  
Beta Adrenergic ◽  
Physiological Importance

To determine the relationship between oxidative capacity and characteristics of beta-adrenergic receptors (beta AR) in skeletal muscle, selected biochemical variables were quantitated in particulate preparations from soleus and gastrocnemius muscle from rats subjected to 10 wk of treadmill running and from three control groups: free-fed, sedentary controls; food-restricted, pair-weighted controls; and animals trained by swimming. Beta AR density and isoproterenol-stimulated adenylate cyclase activity were considerably greater in the slow-twitch oxidative soleus muscle than in the mixed fiber type gastrocnemius in animals from each group (P less than 0.005). Succinic dehydrogenase (SDH) activity of gastrocnemius was increased 23-42% (P less than 0.05) in runners over each of the control groups, concommitantly with a 15-27% increase (P less than 0.05) in beta AR density (Bmax for binding of 125I-cyanopindolol). In 24 animals from all four treatment groups, there was a significant correlation between SDH activity and beta AR density (r = 0.68; P less than 0.001). We conclude that BAR density correlates positively with oxidative capacity in skeletal muscle, but further studies are required to determine the physiological importance of these differences.

scholarly journals You beta block: or not?

2020 ◽  
pp. S59-S61
Author(s):  
L Gilililand
Keyword(s):  
Blood Vessels ◽  
Adrenergic Receptors ◽  
Smooth Muscles ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Β Blockers

β-blockers bind selectively to beta-adrenergic receptors and interfere with catecholamines provoking β-responses on the heart and smooth muscles of the airways and blood vessels. To block or not to block.

scholarly journals PEDF-derived peptide promotes skeletal muscle regeneration through its mitogenic effect on muscle progenitor cells

2015 ◽  
Vol 309 (3) ◽  
pp. C159-C168 ◽  
Author(s):  
Tsung-Chuan Ho ◽  
Yi-Pin Chiang ◽  
Chih-Kuang Chuang ◽  
Show-Li Chen ◽  
Jui-Wen Hsieh ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Cyclin D1 ◽  
Satellite Cell ◽  
Muscle Regeneration ◽  
Muscle Fibers ◽  
Skeletal Muscle Regeneration ◽  
Satellite Cell Proliferation

In response injury, intrinsic repair mechanisms are activated in skeletal muscle to replace the damaged muscle fibers with new muscle fibers. The regeneration process starts with the proliferation of satellite cells to give rise to myoblasts, which subsequently differentiate terminally into myofibers. Here, we investigated the promotion effect of pigment epithelial-derived factor (PEDF) on muscle regeneration. We report that PEDF and a synthetic PEDF-derived short peptide (PSP; residues Ser93-Leu112) induce satellite cell proliferation in vitro and promote muscle regeneration in vivo. Extensively, soleus muscle necrosis was induced in rats by bupivacaine, and an injectable alginate gel was used to release the PSP in the injured muscle. PSP delivery was found to stimulate satellite cell proliferation in damaged muscle and enhance the growth of regenerating myofibers, with complete regeneration of normal muscle mass by 2 wk. In cell culture, PEDF/PSP stimulated C2C12 myoblast proliferation, together with a rise in cyclin D1 expression. PEDF induced the phosphorylation of ERK1/2, Akt, and STAT3 in C2C12 myoblasts. Blocking the activity of ERK, Akt, or STAT3 with pharmacological inhibitors attenuated the effects of PEDF/PSP on the induction of C2C12 cell proliferation and cyclin D1 expression. Moreover, 5-bromo-2′-deoxyuridine pulse-labeling demonstrated that PEDF/PSP stimulated primary rat satellite cell proliferation in myofibers in vitro. In summary, we report for the first time that PSP is capable of promoting the regeneration of skeletal muscle. The signaling mechanism involves the ERK, AKT, and STAT3 pathways. These results show the potential utility of this PEDF peptide for muscle regeneration.

Beta-adrenergic modulation of insulin binding in skeletal muscle

1986 ◽  
Vol 250 (2) ◽  
pp. E198-E204
Author(s):  
B. Webster ◽  
S. R. Vigna ◽  
T. Paquette ◽  
D. J. Koerker
Keyword(s):  
Skeletal Muscle ◽  
Plasma Membrane ◽  
Protein Phosphatase ◽  
Adrenergic Receptors ◽  
Plasma Membranes ◽  
Acute Exercise ◽  
Insulin Binding ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Adrenergic Antagonist

Both a high physiological concentration (13.1 nM) of epinephrine (E) and acute exercise (AEx) have previously been shown to increase 125I-insulin binding in skeletal muscle. To investigate the site and mechanism of the effect of epinephrine on binding and the possible link between epinephrine- and AEx-enhanced insulin binding, we measured insulin binding in three different preparations: 1) crude membranes derived from whole soleus muscle incubated in vitro with 13.1 nM E, 2) crude membranes with E present in the binding assay, and 3) purified plasma membranes with E present. Epinephrine enhanced binding in all three preparations by 169, 144, and 164%, respectively, at low concentrations of insulin but had little effect at high concentrations. Epinephrine, therefore appears to have its effect at the plasma membrane. Propranolol (10 microM), a beta-adrenergic antagonist, blocked E-enhanced insulin binding and when added to crude membranes made from soleus and extensor digitorum longus muscle of AEx rats reversed the increase in binding seen with exercise. This indicates that E-enhanced insulin binding is mediated by beta-adrenergic receptors and that AEx enhances insulin binding via beta-adrenergic receptors. Sodium orthovanadate (3 mM), a phosphotyrosyl-protein phosphatase inhibitor, also inhibited the increase in insulin binding due to E, implying that E may increase insulin binding by activating a phosphotyrosyl-protein phosphatase which decreases the phosphorylation of a plasma membrane protein, presumably the insulin receptor.

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