Skeletal Muscle Receptor Organs

2020 ◽  
pp. 86-92
Author(s):  
Bradley G. Klein
Keyword(s):  
Skeletal Muscle ◽  
Muscle Receptor

Glutamate release in midbrain periaqueductal gray by activation of skeletal muscle receptors and arterial baroreceptors

2003 ◽  
Vol 285 (1) ◽  
pp. H137-H144 ◽  
Author(s):  
Jianhua Li ◽  
Jere H. Mitchell
Keyword(s):  
Skeletal Muscle ◽  
Arterial Pressure ◽  
Glutamate Release ◽  
Periaqueductal Gray ◽  
Triceps Surae ◽  
Muscle Receptor ◽  
Arterial Baroreceptors ◽  
Muscle Receptors ◽  
Afferent Inputs ◽  
Arterial Baroreceptor

We have previously reported that both skeletal muscle receptor and arterial baroreceptor afferent inputs activate neurons in the dorsolateral (DL) and lateral regions of the midbrain periaqueductal gray (PAG). In this study, we determined whether the excitatory amino acid glutamate (Glu) is released to mediate the increased activity in these regions. Static contraction of the triceps surae muscle for 4 min was evoked by electrical stimulation of the L7 and S1 ventral roots in cats. Activation of arterial baroreceptor was induced by intravenous injection of phenylephrine. The endogenous release of Glu from the PAG was recovered with the use of a microdialysis probe. Glu concentration was measured by the HPLC method. Muscle contraction increased mean arterial pressure (MAP) from 98 ± 10 to 149 ± 12 mmHg ( P < 0.05) and increased Glu release in the DL and lateral regions of the middle PAG from 0.39 ± 0.10 to 0.73 ± 0.12 μM (87%, P < 0.05) in intact cats. After sinoaortic denervation and vagotomy were performed, contraction increased MAP from 95 ± 12 to 158 ± 15 mmHg, and Glu from 0.34 ± 0.08 to 0.54 ± 0.10 μM (59%, P < 0.05). The increases in arterial pressure and Glu were abolished by muscle paralysis. Phenylephrine increased MAP from 100 ± 13 to 162 ± 22 mmHg and increased Glu from 0.36 ± 0.10 to 0.59 ± 0.18 μM (64%, P < 0.05) in intact animals. Denervation abolished this Glu increase. Summation of the changes in Glu evoked by muscle receptor and arterial baroreceptor afferent inputs was greater than the increase in Glu produced when both reflexes were activated simultaneously in intact state (123% vs. 87%). These data demonstrate that activation of skeletal muscle receptors evokes release of Glu in the DL and lateral regions of the middle PAG, and convergence of afferent inputs from muscle receptors and arterial baroreceptors in these regions inhibits the release of Glu. These results suggest that the PAG is a neural integrating site for the interaction between the exercise pressor reflex and the arterial baroreceptor reflex.

Interaction between carotid baroreflex and exercise pressor reflex depends on baroreceptor afferent input

1998 ◽  
Vol 274 (5) ◽  
pp. H1841-H1847 ◽  
Author(s):  
Jeffrey T. Potts ◽  
Jianhua Li
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Carotid Sinus ◽  
Cardiovascular Responses ◽  
Afferent Input ◽  
Muscle Stretch ◽  
Exercise Pressor Reflex ◽  
Muscle Receptor ◽  
Pressor Reflex ◽  
Passive Muscle

Because arterial baroreceptor and skeletal muscle receptor afferents project to cardiovascular regions in the lower brain stem such as the nucleus tractus solitarii (NTS), it is likely that the level of baroreceptor afferent input will modify the excitatory cardiovascular responses evoked by contraction-sensitive skeletal muscle afferents. The purpose of this study was to determine the effect of carotid sinus baroreceptor afferent input (CSA) on reflex heart rate (HR) and mean arterial pressure (MAP) responses evoked by activation of skeletal muscle receptor afferents (SMA). CSA input was servo controlled at three levels of carotid sinus pressure using the isolated carotid sinus preparation, and SMA input was varied by induced muscle contraction (L7-S1ventral root stimulation) or passive muscle stretch. Experiments were performed in α-chloralose-anesthetized and vagotomized dogs ( n = 9). When CSA input was low (106 ± 35 mmHg), electrically induced muscle contraction increased HR and MAP (30 ± 8 beats/min and 42 ± 12 mmHg, respectively, P < 0.05). However, when CSA input was high (221 ± 9 mmHg), the reflex changes in HR and MAP during muscle contraction were attenuated (6 ± 4 beats/min and 18 ± 4 mmHg, respectively, P< 0.05). Similarly, the sympathoexcitatory responses evoked by passive muscle stretch were attenuated in a baroreceptor-dependent manner. These results suggest that changing CSA input from low (106 mmHg) to high (221 mmHg) shifts the interaction from facilitation to inhibition. Therefore, it is concluded that the nature of the interaction (i.e., facilitation or inhibition) between the baroreflex and the exercise pressor reflex is dependent on the level of baroreceptor input. Moreover, our findings substantiate early studies showing that the level of afferent input from arterial baroreceptors is a powerful modulator of sympathoexcitation evoked by mechanically and metabolically sensitive skeletal muscle receptors.

Identification of the cAMP-Specific Phosphorylation Site of the Purified Skeletal Muscle Receptor for Calcium-Channel Blockers

1989 ◽  
Vol 560 (1 Calcium Chann) ◽  
pp. 395-397 ◽  
Author(s):  
A. RÖHRKASTEN ◽  
W. NASTAINCZYK ◽  
H. E. MEYER ◽  
M. SIEBER ◽  
T. SCHNEIDER ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Phosphorylation Site ◽  
Channel Blockers ◽  
Muscle Receptor

Endotoxin Alteration of the Mucopolysaccharide Blood Vessel Coating in Rats

1974 ◽  
Vol 32 ◽  
pp. 148-149
Author(s):  
D. E. Philpott ◽  
A. Takahashi
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Cells ◽  
Salivary Gland ◽  
Carotid Artery ◽  
Basement Membrane ◽  
Coronary Vessels ◽  
Ruthenium Red ◽  
E Coli ◽  
Old Rats ◽  
The Brain

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.

Ultra-Rapid Freezing of Isolated Skeletal Muscle Fibers

1977 ◽  
Vol 35 ◽  
pp. 576-577
Author(s):  
Joachim R. Sommer ◽  
Nancy R. Wallace
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Granular Material ◽  
Nuclear Envelope ◽  
Intracellular Calcium ◽  
Ruthenium Red ◽  
Threshold Concentration ◽  
Rapid Freezing ◽  
Frog Skeletal Muscle ◽  
Electrical Isolation

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.

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