scholarly journals Evidence for centrally induced cholinergic vasodilatation in skeletal muscle during voluntary one-legged cycling and motor imagery in humans

2013 ◽  
Vol 1 (4) ◽  
Author(s):  
Kei Ishii ◽  
Kanji Matsukawa ◽  
Nan Liang ◽  
Kana Endo ◽  
Mitsuhiro Idesako ◽  
...  
2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Kei Ishii ◽  
Kanji Matsukawa ◽  
Nan Liang ◽  
Kana Endo ◽  
Mitsuhiro Idesako ◽  
...  

1965 ◽  
Vol 208 (3) ◽  
pp. 417-424 ◽  
Author(s):  
Lawrence D. Dorr ◽  
Michael J. Brody

The hypothesis that sympathetic innervation to skeletal muscle vasculature contains functionally distinct adrenergic and cholinergic fibers was investigated utilizing the dog isolated perfused gracilis muscle. The use of hemicholinium in an attempt to abolish cholinergic dilatation, but not adrenergic constriction, in response to intermittent nerve stimulation was not successful. Continuous nerve stimulation produced vasoconstriction which was maintained for the duration of stimulation. Conversely, when cholinergic vasodilatation was unmasked, continuous stimulation resulted in a dilator response which disappeared rapidly. These experiments suggested that release of the adrenergic transmitter could not be dependent upon an intermediate cholinergic link in the sympathetic nerve. This postulate was supported further by experiments utilizing electrical stimulation of medullary vasoconstrictor areas. Whereas cholinergic vasodilatation was unmasked routinely by peripheral stimulation following reserpine, guanethidine or ß-TM 10, this response was never seen when medullary vasoconstrictor neurons were activated following these agents. It was concluded that sympathetic cholinergic nerves to skeletal muscle vessels possess a purely vasodilator function, and do not play an intermediate role involving release of the adrenergic transmitter.


Author(s):  
D. E. Philpott ◽  
A. Takahashi

Two month, eight month and two year old rats were treated with 10 or 20 mg/kg of E. Coli endotoxin I. P. The eight month old rats proved most resistant to the endotoxin. During fixation the aorta, carotid artery, basil arartery of the brain, coronary vessels of the heart, inner surfaces of the heart chambers, heart and skeletal muscle, lung, liver, kidney, spleen, brain, retina, trachae, intestine, salivary gland, adrenal gland and gingiva were treated with ruthenium red or alcian blue to preserve the mucopolysaccharide (MPS) coating. Five, 8 and 24 hrs of endotoxin treatment produced increasingly marked capillary damage, disappearance of the MPS coating, edema, destruction of endothelial cells and damage to the basement membrane in the liver, kidney and lung.


Author(s):  
Joachim R. Sommer ◽  
Nancy R. Wallace

After Howell (1) had shown that ruthenium red treatment of fixed frog skeletal muscle caused collapse of the intermediate cisternae of the sarcoplasmic reticulum (SR), forming a pentalaminate structure by obi iterating the SR lumen, we demonstrated that the phenomenon involves the entire SR including the nuclear envelope and that it also occurs after treatment with other cations, including calcium (2,3,4).From these observations we have formulated a hypothesis which states that intracellular calcium taken up by the SR at the end of contraction causes the M rete to collapse at a certain threshold concentration as the first step in a subsequent centrifugal zippering of the free SR toward the junctional SR (JSR). This would cause a) bulk transport of SR contents, such as calcium and granular material (4) into the JSR and, b) electrical isolation of the free SR from the JSR.


Author(s):  
A. V. Somlyo ◽  
H. Shuman ◽  
A. P. Somlyo

Electron probe analysis of frozen dried cryosections of frog skeletal muscle, rabbit vascular smooth muscle and of isolated, hyperpermeab1 e rabbit cardiac myocytes has been used to determine the composition of the cytoplasm and organelles in the resting state as well as during contraction. The concentration of elements within the organelles reflects the permeabilities of the organelle membranes to the cytoplasmic ions as well as binding sites. The measurements of [Ca] in the sarcoplasmic reticulum (SR) and mitochondria at rest and during contraction, have direct bearing on their role as release and/or storage sites for Ca in situ.


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