Flashcards in Muscle Excitation and Signaling and Contraction Deck (23):
At what voltage do Na+ activation gates open?
-70 to -20mV
At what voltage do Na+ inactivation gates open?
-80 to -40mV (at -40, most will be closed)
What happens with Na+ channels if the cell's resting potential is depolarized?
More inactivation Na+ channels will be closed, and less will be available to allow Na+ flow up to threshold
-this occurs in ischemia, infarction, inc K+, TTX
What is an M gate
Activation Na channel
What is an H gate?
M/H positions at resting potential
M/H positions at upstroke
M/H positions at Plateau
At what voltage does phase 4 depol occur in SA node?
-70 to -50mV
What does the ST segment represent?
At what voltage does purkinje fiber phase 4 depol occur?
-90 to -70mV
What determines the amplitude of electrical vectors?
1. Mass of muscle
2. Conduction velocity
3. Degree of cancellation of electrical forces
NOT the rate of phase 4 depol
What is similar about contraction and relaxation of myosin?
Both are energy dependent!
-->ATP req to disassociate myosin from thin filament
-->ATP req to pump Ca2+ back into SR
How is Ca2+ removed from the myoplasm?
1. Ca2+ pump: active transporter on SR membrane
2. Na+/Ca2+ exchanger pumps in 3 Na+ for 1 Ca2+ out of the cell, operates on Na+ electrochemical gradient
3. 3Na+ out/2K+in exchanged via ATPase
What's the difference between Ca2+ activation in skeletal vs cardiac muscle?
In cardiac: ca induced ca release (via L type Ca channels). Muscle is activated via Ca from SR and from EC space. Ca is also pumped back out into EC space. Muscle can only stay contracted for as long as Ca is there.
In skeletal: Voltage dependent and only pumps out of SR and then back into SR. doesnt leave cell space, calcium doesn't come from outside space. Muscle can stay contracted for longer than Ca is there
What is twitch duration controlled by in cardiac vs skel m
Cardiac: AP duration
Skel: not AP duration
What 3 mechanisms dec HR?
1. Reduce rate of phase 4 depol
2. Less neg threshold (takes longer to get there)
3. More neg max diastolic pot (ie lower resting potential)
How does vagus regulate HR?
Ach binds K+ channel and allows more K+ out of the cell
How does SNS regulate HR
Norepi and epi bind GPCRs leading to increase in Ca2+ current and increased rate of diastolic depol
What regulates strength of contraction?
1. Amt of Ca2+ in the cell and response to Ca2+
-->faster heart beats, stronger beats are because Ca2+ doesn't have time to leave the area
2. Concentration of Na+
-->cardiac cells contract more strongly with reduced Na+ because it dec efficacy of Na/Ca2+ exchanger
3. Concentration of K+
-->If you increase concentration of K+, you shorten the AP because you increase the resting potential
4. Catecholamine regulation
-->Inc cAMP leads to phosphorylation of phospholamban which increases the rate of Ca2+ uptake into the SR
-->Increase strength of contraction by inc magnitude of activator Ca2 current into cell
-->Decrease duration of contraction by inc SERCA pumping and phosphorylating troponin I and dec its affinity for Ca2+ (modulates other effects of catecholamines)
Explain Frank-Starling law
Greater T = greater F of contraction
-stretch=closer thick/thin filaments making easier for myosin to generate greater F
Role of phospholamban
Normally inhibits SERCA. Inactivated when phosphorylated. Normally inactivated via catecholamine regulation