Flashcards in Cardiac Muscle: Control of Myocardial Contraction Deck (16):
Surface membrane + SR membrane = ?
SR membrane + T-tubule membrane = ?
(I doubt this is really important, but it is important to their function that they're in close proximity to each other)
What are Ryanodine receptors? What makes them open?
Ca++ channels on the SR membrane that open in response to calcium flowing in from T-tubules through L-type Ca++ channels (aka DHPR).
What does tropomyosin do?
It sits on actin and prevents myosin from binding unless Ca++ is present.
How do skeletal and cardiac muscle contrast in the effect of Ca++ on ryanodine receptors?
Cardiac muscle is dependent on extracellular calcium flowing into the cells through L-type Ca++ channels (DHPRs), then binding ryanodine receptors, causing them to open.
(In skeletal muscle, Ca++ allows the DHPRs to directly contact the ryanodine receptors, causing them to open.)
3 ways to slow the pacemaker rate?
Reduced rate of phase 4 depolarization.
(i.e. slow depolarization by T-type Ca++ channels takes longer)
Higher threshold for Phase 0 depolarization.
Lower minimum potential.
(obviously, doing the reverse will increase the pacemaker rate)
How does the sympathetic nervous system speed up heart rate?
Catecholamines -> GPCR (Gs) -> cAMP -> PKA -> phosphorylation (activation) of T-type Ca++ channels ->
Faster phase 4 depolarization.
How does the parasympathetic nervous system slow down heart rate?
ACh -> muscarinic receptor (GPCR) -> activation of K+ channel -> hyperpolarization of pacemaker cells
(also Gi inhibits adenylyl cyclase -> less cAMP -> less activation of T-type Ca++ channels)
3 ways to increase strength of contraction in cardiac myocytes?
Increase sensitivity to Ca++.
Increase force generated by change in [Ca++].
What happens intrinsically to contraction strength if heart rate increase?
Contraction strength increases.
Why does Ca++ build up in cardiac myocytes at faster heart rates? Effect?
Systole (Ca++ influx) duration doesn't change much, but diastole (Ca++ efflux) duration decreases, leading to Ca++ buildup in both the cytoplasm and SR.
Increased [Ca++] -> stronger contractions.
Does the strength of contraction vary with how much blood comes in during diastole?
Yup, it increases. (Frank-Starling Law of the Heart)
(this flashcard brought to you my cat)
What's the molecular mechanism for why contractions get stronger with increased filling?
Stretching makes the sarcomeres change shape such that myosin heads make better contact with actin.
What effect does cAMP actually have on myocytes' sensitivity to Ca++?
cAMP actually decreases myocytes' sensitivity to Ca++, but there's so much Ca++ that there's a net increase in contraction strength.