Biochemical change in muscle contraction Flashcards
3 types of muscle
-skeletal mscl
-smooth mscl
-cardiac mscl
what is sarcomere
thick an thin filament in myofibril
-thick filaments are contractile proteins myosin
-thin filament are contractile proteins actin, troponin and tropomysin
monomeric form of actin?
G- actin polymerizes in the presence of mg to form an insoluble double helical filament called F-actin
F-actin
Each F actin molecule has an active site to which the myosin head is attached.
About 40 to 60 tropomyosin molecules are situated along the double helix strand of actin filament. In relaxed condition of the muscle, the tropomyosin molecules cover all the active sites of Factin molecules.
troponin I- Factin
troponin T- tropomysin
troponin c-ca
myosin
-thick filament
- 2 large polypeptide heavy head
-4 smaller light chain
- 2 globular head and long tail(cross bridge)
-each head (1atp n 1 actin binding site)
T tubules
Ttubules or transverse tubules are narrow tubules formed by the invagination of the sarcolemma. These tubules penetrate all the way from one side of the muscle fiber to an another side.
L tubule
Ltubules or longitudinal tubules are the closed tubules that run in long axis of the muscle fiber, forming sarcoplasmic reticulum. These tubules form a closed tubular system.
muscle contraction
1.release ca ion from cisternae of L tubules
2. binding of calcium ion with troponin
3.change in position of troponin
4. pulling of tropomyosin molecules away from f actin
5. exposure of active site of F actin
6.attachment of myosin head to actin
7. power stroke- tilting of myosin head and drag actin filament
8.detach myosin head and return original position
9.attachment of myosin head to new active site of F actin and drag actin filament
10. contraction of muscle
sarcoplasmic reticulum regulates intracellular level of ca in skeletal muscle
CONTRACTION
- ca is pumped into the SR through the action of active transport, Ca ATPase ,initiate release
2.inside SR, ca bound specific ca binding protein designated calsequestrin
3.sarcolemma is excited by nerve impulses, signal transmit into T tubule and ca release channel in nearby sarcoplasmic reticulum release ca . calcium release channel also known as ryanodine receptor
4.concentration of ca in sarcoplasm rises rapidly. ca binding site on troponin c in the filament.
5.the tp c - ca interact with tp I and tp T to alter interactions with tropomysin - tropomyosin alter conformation of F-actin so that so that myosin head ADP-Pi can interact with F-actin to start the contraction cycle
sarcoplasmic reticulum regulates intracellular level of ca in skeletal muscle
RELAXATION
- SR ca falls owing to its resequestration into SR by Ca ATPase
2.Tp c loses its ca. also troponin inhibit further myosin head and F-actin interactions, in the presence of ATP the myosin head detaches from the F-actin - ca control skeletal muscle contraction n relaxation by an allosterix mechanism mediated by TpC, TpI , TpT , tropomysin and F-actin
Myosin- based regulation occur in smooth muscle
- T tubule absent, L tubule poorly developed
- excitation and contraction slow
- so, ca ion that responsible for excitation-contraction coupling, must obtain from ecf
Smooth muscle CONTRACTION
In smooth muscle, the myosin has to b e phosphorylated for the activation of myosin ATPase. Phosphorylation of myosin occursin thefollowing manner:
- At low concentrations of Ca2+, c a l d e s m o n (calmodulin binding protein) bindsto tropomyosin and actin., thereby prevents interaction of actin with myosin, keeping muscle in a relaxed state.
- At higher concentrations of Ca2+, Calcium, which enters the sarcoplasmf r o m the extracellular fluid combines with a protein called calmodulin and forms calcium-calmodulin complex.
3.This Ca2+-calmodulin binds caldesmon, therefore releasing caldesmon fromactin.
4.The latter is then free to bind to myosin, and contraction can occurbyactivates calmodulin-dependentmyosin lightchain kinase.
5.This enzyme in turn causes phosphorylation of myosin followed by activation of myosin ATPase.Now,theslidingof actin filamentsstarts.
smooth muscle RELAXATION
• Upon diffusing into the surrounding vascular smooth muscle cells, NO binds to the haeme moiety of a soluble guanylyl cyclase.
• It activates the enzyme and elevating the intracellular levels of the second messenger 3’,5’-cyclic GMP (cGMP).
• This in turn stimulates the activities of certain cGMP dependent protein kinases, which probably phosphorylate specific muscle proteins, causing relaxation.
regulation of contraction in cardiac muscle
The Ttubular system is more developed in cardiac muscle, whereas the SR is less extensive and consequently the intracellular supply of Ca2+ for contraction is lower. Cardiac muscle thus relies on extracellular Ca2+ for contraction.
Ca2+ Enters Cardiomyocytes via Ca2+ Channels & leaves via the Na+-Ca2+ Exchanger & the Ca2+ ATPase
• Extracellular Ca2+ enters cardiomyocytes via L-type or slow Ca2+ channel, which is voltage-gated.
• Slow Ca2+ channels are regulated by cAMPdependent protein kinases (stimulatory) and cGMP- dependent protein kinases (inhibitory).
• Fast (or T, transient) Ca2+ channels are also present in the plasmalemma, though in much lower numbers and contribute to the early phase of increase of myoplasmic Ca2+.
• When the concentration of Ca2+ in the myoplasm increases, it triggers the opening of the Ca2+ release channel of the SR and is called Ca2+-induced Ca2+ release.
cardiac muscle relaxation
Relaxation: The Na+-Ca2+ exchanger: Na+ and Ca2+ are exchanged with movement of sodium ions into the cell from the plasma providing the energy needed to move calcium into the plasma against a concentration gradient. This exchange contributes to relaxation.
