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Introduction to Musculoskeletal System

Typology: Lecture notes

2017/2018

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Introduction to Musculoskeletal System 55
1 4
6 D
1 7
7 7
4 7
Neuromuscular Transmission & Mechanisms of Contraction
of Skeletal Muscle
1. 7 5
3 1
nerve 5 2
3 A
6 F
C 0
5 B
E B
5 2
3 0
muscle 65
3 6
7 E
2 E
1..i action potential arrive presynaptic terminal F0
E 0
Ca+
+ channel open F0
E 0
Ca++ rush in (electrochemical
gradient) F 0
E 0
release of Ach from synaptic vesicles into the
synaptic cleft by exocytosis F 0
E 0
diuse to muscle membrane
(sarcolemma) and bind to its receptors’ α subunits)
receptor= nicotinic receptor F 0
E 0
Na+ and K+ ion channel
open F 0
E 0
produce end plate potential F 0
E 0
summate ~
threshold ~ action potential F0
E 0
action potential is
conducted along t-tubules F0
E 0
activate votage-gated Ca++
channel ,called dihydropyridine receptor ( in t-tubules) F 0
E 0
Ca++ release channel open (in SR, sarcoplasmic
reticulum) F 0
E 0
Ca++ release to sarcoplasm, bind to
troponin, stimulate contraction
2. 15 0
0 B
synaptic vesicle produce 76
8 4
potential 53
E B
miniature potential
3. Synthesis and of Ach:
Choline acetyltransferase
3..i Acetyle coenzyme A + choline --------------------------
> acetylcholine
4. Degradation of Ach:
Acetylcholinesterase
4..i Acetylcholine --------------------------------> acetyle
coenzyme A + choline
5. Properties of Muscle ( 3 5 0
0 B
“easy” F0
E 0
EC)
5..i Excitability
5..ii Extensibility
5..iii Elasticity
5..iv Contractility
6. Organization of skeletal muscle:
6..i Myobrils F 0
E 0
Muscle bers F 0
E 0
Muscle
fascicles F 0
E 0
Skeletal muscles
6..ii F0
E 0
Sarcolemma
+endomysium F 0
E 0
Perimysium F 0
E 0
Epimysium
7. 8 0
8 C
8 0
8 9
6 5
3 6
7 E
2 E
6 6
4 2
, A band 9 5
7 7
5 E
A 6
4 E
0 D
8 B
8 A
, Z lines 95
9 3
8 D
D D
9 6
E 2
7 E
2 E
7 7
E D
pf3
pf4

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Introduction to Musculoskeletal System 5 51 46 D1 77 74 7 Neuromuscular Transmission & Mechanisms of Contraction of Skeletal Muscle

  1. 7 53 1nerve 5 23 A6 FC 05 BE B5 23 0muscle 6 53 67 E2 E 1..i action potential arrive presynaptic terminal F 0E 0 Ca+ + channel open F 0E 0 Ca++ rush in (electrochemical gradient) F 0E 0 release of Ach from synaptic vesicles into the synaptic cleft by exocytosis F 0E 0 diffuse to muscle membrane (sarcolemma) and bind to its receptors’ α subunits) receptor= nicotinic receptor F 0E 0 Na+ and K+ ion channel open F 0E 0 produce end plate potential F 0E 0 summate ~ threshold ~ action potential F 0E 0 action potential is conducted along t-tubules F 0E 0 activate votage-gated Ca++ channel ,called dihydropyridine receptor ( in t-tubules) F 0E 0 Ca++ release channel open (in SR, sarcoplasmic reticulum) F 0E 0 Ca++ release to sarcoplasm, bind to troponin, stimulate contraction
  2. 1 5 00 Bsynaptic vesicle produce 7 68 4 potential 5 3E Bminiature potential
  3. Synthesis and of Ach: Choline acetyltransferase 3..i Acetyle coenzyme A + choline --------------------------

acetylcholine

  1. Degradation of Ach: Acetylcholinesterase 4..i Acetylcholine --------------------------------> acetyle coenzyme A + choline
  2. Properties of Muscle ( 3 5 00 B “easy” F 0E 0EC) 5..i Excitability 5..ii Extensibility 5..iii Elasticity 5..iv Contractility
  3. Organization of skeletal muscle: 6..i Myofibrils F 0E 0Muscle fibers F 0E 0Muscle fascicles F 0E 0Skeletal muscles 6..ii F 0E 0Sarcolemma +endomysium F 0E 0Perimysium F 0E 0Epimysium
  4. 8 08 C8 08 96 53 67 E2 E6 64 2 , A band 9 57 75 EA 64 E0 D8 B8 A , Z lines 9 59 38 DD D9 6E 27 E2 E7 7E D
  1. Thick filaments contain myosin , Thin filaments contain 3 proteins: actin , troponin ,tropomyosin
  2. **Excitation–contraction coupling in skeletal muscle / cross- bridge cycle 9..i Ca2+ binds to troponin C on the thin filaments, causing a conformational change in troponin that moves tropomyosin out of the way. The cross-bridge cycle begins 9..ii The cross-bridge heads function as ATPase enzymes 9..iii ATP is hydrolysed to ADP and P i , activating the cross bridge 9..iv When the activated cross bridges attach to actin, they release P i and undergo a power stroke 9..v At the end of a power stroke, the cross bridge releases the ADP and binds to a new ATP 9..vi This allows the cross bridge to detach from actin and repeat the cycle’ 9..vii Rigor state is caused by the inability of cross bridges to detach from actin because of a lack of ATP

t-tubules 5 40 C SR 7 68 49 5D C4 FC 2: 10..i

10..ii Action potential 5 23 0 t-tubules , activate dihydropyridine receptor ( 9 02 34 F4 FSR 6 79 C5 00 B Ca++ release channel) , 6 24 04 EE 5open ,then Ca++ release to sarcoplasm, bind to troponin, stimulate contraction 8 A7 38 98 B1.

afferent arterioles dilate when the mean arterial pressure falls toward 70 mmHg, and the afferent arterioles constrict when the mean arterial pressure rises above normal. Blood flow to the glomeruli and GFR can thus remain relatively constant within the autoregulatory range of blood pressure values. Two general echanisms are responsible for renal autoregulation: (1) myogenic constriction of the afferent arteriole, due to the ability of the smooth muscle to sense and respond to an increase in arterial pressure; and (2) the effects of locally produced chemicals on the afferent arteriole, which is part of a process called tubuloglomerular feedback. The sensor in tubuloglomerular feedback is macula densa, located in the thick portion of the ascending limb where it comes in contact with the afferent and efferent arterioles in the renal cortex. When there is an increased delivery of NaCl and H2O to the distal tubule (as occurs when increased arterial pressure causes a rise in the GFR), the macula densa sends a chemical signal causing constriction of the afferent arteriole. This reduces the GFR so that less fluid enters the nephron tubules, a response that protects the late distal tubule and cortical collecting duct from becoming overloaded.