Muscle Pt. 7 (Cardiac-EC coupling/relaxation/contracile vs autorythmic) Flashcards
What is the funciton of cardiac muscle?
to contract & create pressure gradient to allow bloodflow
Cardiac muscle made of cardiac myocytes, which are __ myofibrils than SM
shoerter fibers, stacked on top of eachother
Cardiac myocytes are . . .
branched cells that usually only have 1 nucleus
Cardiac muscle is interconnected by _____. What is the benefit? (what 2 parts make these up?)
connected via interclated disks = seperate cells
interclated disks = allows uniform contraction in chamber
1. desmosomes = link cells mechanically
2. gap junctions = links cells electrically
T/F Cardiac muscle is not straited
does it have thick/thin filaments?
False - cardiac muscle = striated with similar thin/thick filamnts
Do cardiac muscle have T-tubules?
Yes, less abundant (compared to SM) but do form a network
T-tubules run un random directions (unlike SM = only parralel)
Cardiac muscle has a ___ SR compared to SM
smaller SR
Cardiac muscle requires the entry of EXTRACELLULAR Ca+ = doesn’t need Ca storage
Cardiac muscles relationship to mitochondria
mitochondria make up 1/3 of cell volume
allows cardiac to use oxidative metabolism for ATP protuctino
T/F cardiac muscle perform a lot of work contineuosly
True = contact about 3 billion times in lifespan
Is contraction started by nueros in cardiac muscle?
No!!! nueral input in cardiac can only MODIFY contraction not CREATE it (unlike SM)
Skeletal muscle has a __ AP within its __ period.
SM = brief AP in latent period
allows for multiple AP to be generated and summed for greater tension
Cardiac muscle has ___ AP and a ___ period
Cardiac muscle = eleongated AP & refractory period
long AP prevents summation of AP within the same period (would lead to more contraction force) & we need the heart to relax between contractions
How does EC coupling in cardiac muscle differ from that of skeletal?
Cardiac = L-type Ca+ channels (DHP channels) are NOT linked to RyR receptors —> DEPENDING on Ca+ entry from EXTRACELLULAR for contraction
SM = they were linked
Through what proccess is extracellular Ca+ aquired in cardiac muscles
Ca+ induced Ca release
How is relaxation done for cardiac muscle?
Cardiac muscle needs to return about 10% of Ca+ signal it received from the extracellular space
and return 90% of Ca signal it received from SR
What is the primary mechanism of cardiac muscle relaxation?
reuptake into the S is still the primary method
How does Ca+ uptake into SR differ in cardiac from skeletal?
skeletal = SERCA pump allways highly active
cardiac = SERCA pump controled by phospholamban (phosphorylated = high uptake = fast relax & unphosphorylated = low uptake)
How do you enhance contractile force in cardiac muscle?
how does this differ from skeletal muscle?
Cardiac
1. increase in intracellular Ca+ in myocytes = increase force (due to graded single twitch capability, low cystolic Ca+ level, and increased Ca+)
2. Length tension relationship = cardiac muscle generaters a greater force when slighly streched (ulike optimal length of skeletal)
skeletal muscle force was increased via increase in AP = summation/tetanus
Exaplain how nueronal input on the Cardiac muscle (the heart) can modify conduction/contraction
Heart is intervated by the autonomic nervous system
Sympathetic activity/input (fight/flight) = controls both autoryhtmic cells (increase heart rate/conduction) and contractile cells (increase in contracility)
Paraysympathetic input (rest) = controls ONLY autorythmic (decrease heart rate/conduction)
symp imput (active) = increase heart rate/conduction (autorythmic) & increase contractility (contractile)
parasymp input (rest) = decrease heart rate/conduction (autorythmic)
List 4 mechanisms that create an increase/start sympathetic modulation in Cardiac
- increased extracellular Ca+ entering (increase conductance via phosphorylation of L-type Ca+ chanels)
- increase release of Ca+ from SR (via phosphorylization of RyR receptors)
- Increase rate of myosin ATPase
- Increase Ca+ reuptake speed (via phosphorylation of SERCA pump)
2nd way to increase force in cardiac
What is the Cardiac length tension releationship?
ability of cardiac to make more contraction even when lightly streched (unlike optimal SM length)
1. strech -> smalled diameter –> shortens travel time for Ca+ across
2. strech –> adds more tension on stress-activated Ca= channels = increase Ca+ entry from Extracellular
What is the normal instrinsic firing rate of autorythmic cells without autonomic input?
90 AP/min for auto cells in SA node (sympa input = increase ) (parasympa = decrease)
in resting state, parasmpatheitc is more dominant = 70-72 BPM
What is the normal instrinsic firing rate of autorythmic cells without autonomic input?
90 AP/min for auto cells in SA node (sympa input = increase ) (parasympa = decrease)
in resting state, parasmpatheitc is more dominant = 70-72 BPM
How does parasympathetic input modulate pacemaker activoty?
they decrease frequency of AP at the SA and AV node = decrease heart rate there
= act as decrease in conduction veloiity at AV node
parasypathetic modulation of pacemaker activty
Name 3 mechanisms that decrease conduction velocity at AV node?
- slow opeing of HCN chanenels (vs fast)
- opening of K+ GIRK channels
- block T-type Ca+ channels
List 3 ways that sympathetic input can modulate pacemaker activity
- activate beta1 adregenic receptors (by NE/Ep) –> increase Na & Ca entry through channels –> cells reach threshold faster –> with a decreased level of repolarization = RAPID AP firing
