Muscle Flashcards
explain the following for skeletal muscle:
- termination of contraction
- twitch duration
- regulation of force
- metabolism
- termination of contraction is acetlcholinesterase enzyme degrading Ach
- twitch duration is 20-200msec
- regulation of force is frequency and multi fiber summation
- metabolism is oxidative and glyocolytic
explain the following for smooth muscle:
- termination of contraction
- twitch duration
- regulation of force
- metabolism
- termination of contraction with myosin light chain phosphotase
- 200 msec sustained twitch duration
- force regulated by balance of MLCK phosphate and dephosphate and latch state
- metabolism is oxidative
explain the following for cardiac muscle:
- termination of contraction
- twitch duration
- regulation of force
- metabolism
- terminate contraction with A.P. repolarization
- 200msec- 400 msc
- force regulated by calcium entry
- metabolism is oxidative
explain excitation coupling, electrical activity and mechanism of excitation for skeletal, cardiac, and smooth muscle
skeletal:
- Ltype Ca++ channels in t tubules are physically coupled to Ca++ release in SR
- A. P spikes
- excitation via neuromuscular transmission
smooth:
- Ca+ voltage gated channels allow calcium in to bind IP3 to release more calcium. Calcium entry via SOCC
- AP spikes and plates with short waves
- excitation via synaptic transmission/hormone/electrical coupling/pacemaker
cardiac:
- L type Ca++ channel triggers release from SR
- AP spikes
- pacemaker depolar via gap junctions
for skeletal, cardiac, and smooth. which receptor releases SR calcium and which receptor is linked to it?
in smooth:
IP3 is receptor and it is linked in the membrane to avoltage gated channel.
in cardiac:
-have ryanodine receptor linked to voltage gated
in skeletal:
-have rynaodine receptor linked to dihydropyridine receptor in t tubule
how is it that calcium can be needed or cannot be needed for contraction in muscle
MLCK phosphorylates the myosin chain and MLCP takes off the phosphate.
HOwever, if we phosphorylate MLCP, it can’t take off the phosphate so the myosin stays active. this is done by RhoA kinase.
also , can have cGMP which doesn’t need calcium to activate MLCP (think viagra)
describe the mechanism of action for viagra
during muscle relaxation, nitrous oxide pathway stimulates guanyl cyclase to produce cGMP. this activates cGMP dependent protein kinase PKG that causes smooth muscle to relax.
viagra inhibits the breakdown of cGMPby PDE5 phosphodiesterase to enhance the NO/cGMP interaction.
for skeletal, smooth, and cardiac, what is needed to initiate and continue the contraction?
smooth: phosphate dissociation from myosin inhibited at low calcium. to start also need calmodulin to bind calcium to activate MLC.
in straited muscle, phosphate dissociation inhibited at low calcium
for skeletal: once myosin hydrolyses ADP+Pi, the actin moves the P off for the power stroke and then Myosin and Actin are stuck until ADP released
in cardiac???
which muscle has greatest force of contraction?
cardiac, then smooth, then muscle
Which of the following mechanisms is a common feature of the regulation of cardiac and skeletal muscle contraction?
. Calcium dependent calcium release
-different RYR channels eh?
how is beta adrenergic stimulation important for cardiac cycle contraction?
increase in sympathetic activity increase NE, increases activation of beta adrenergic receptors. turns up the volume!
how does troponin of skeletal and cardiac differ and why is this important?
troponin for skeletal is shorter. TnI of cardiac muscle has an serine residue that is phosphorylated during sympathetic activation
This leads to a decrease in calcium sensitivity of the Tn complex and to Ca2+ more rapidly moving OFF of the Tn complex (aids in increasing lusitropy)
increase in heart rate , contractility, and relaxation rate are called?
lusitropy is relaxation rate
ionotropy is contractility
chronotropy is heart rate
troponin binding in skeletal vs cardiac
troponin binds Ca in skeletal. in cardiac, tropnin has subunits and the C binds calcium, I is inhibitory and T binds tropmyosin.
steric hinderance is due to troponin-tropomysoin complex inhibiting P release (remember for smooth muscle, need MLCP for phosphate release)
RYR1 vs RYR2 disease
RYR 1: in skeletal muscle gives malignant hyperthermia. so this is a autosomal myopathy. triggered by anesthesia or neuromuscular blockers.
RYR 2 in cardiac muscle gives hypertrophy and heart failure . why? reduction in RYR channels
