L10 Myocardial E-C Coupling Flashcards

0
Q

Functional role of T Tubule

A

transmits electrical activity to the cell’s interior; located at Z lines

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1
Q

Functional role of Sarcolemma

A

propagates the AP down into the T tubule; Contains L-type Ca channels so controls Ca influx

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2
Q

Functional role of SR

A

Site of Ca storage
Terminal Cisternae is where CICR occurs to initiate contraction
Longitudinal Cisternae is where SERCA functions to take Ca back into the cell for relaxation

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3
Q

Functional role of Troponin C

A

Binds Ca when it’s available and moves the Tropomyosin/Troponin into the actin groove so actin/myosin can affiliate for contraction

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4
Q

Troponin/Myosin in Heart

A

is the same as in skeletal muscle. Same contraction mechanisms

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5
Q

Cellular mechanisms in E-C Coupling

A
  1. Impulse from pacemaker cell conducts down cell and is carried into the cell by T Tubules
  2. Depolarization causes slow inward Ca current via L-type Ca channels
  3. Ca in the cell can now bind and open RyR channels
  4. Ca released from SR and binds to Troponin-C
  5. actin-myosin motion
  6. SERCA takes Ca back into SR
  7. Ca also removed via Na/Ca exchange and random Sarcolemma pump
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6
Q

Cardiac vs. Skeletal: size

A

Cardiac: small

Skeletal: large

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7
Q

Cardiac vs. Skeletal: innervation

A

Cardiac: all innervated in syncytium – coupled via gap connections

skeletal: all cells innervated separately

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8
Q

Cardiac vs. Skeletal: electrical activation

A

Cardiac: cell-cell conduction

skeletal: NMJ using Ach

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9
Q

Cardiac vs. Skeletal: contraction with Ca

A

Cardiac: uses CICR with Ryr

Skeletal: voltage dependent DHPR activates RyR
doesn’t require Ca, requires voltage to be depolarized

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10
Q

Cardiac vs. Skeletal: contraction amplitude

A

Cardiac: larger amplitude = regulated by Ca influx in L-type and Ca content in SR

Skeletal: larger amplitude = frequency of APs summated and recruitment of more fibers

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11
Q

Cardiac vs. Skeletal: metabolims

A

Cardiac: aerobic; requires O2 -> 35% mitochondria

Skeletal: anaerobic -> 2% mitochondria
never infarcts

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12
Q

Factors that change contraction via changing Contractility: Catecholamines

A

NE, ie. - decreases time of relaxation & increases strength of contraction
positive inotropic effect - (definition of positive inotropic agent = something that increases CONTRACTILITY)

bind to B1 receptors, which make cAMP from ATP
cAMP activates PKA, which P’s *Ca channels (increases contraction strength by increasing influx), *phospholamban (enhances relaxation by enhancing SERCA activity), *Troponin-I, (enhances relaxation by inhibiting the binding of Ca to Troponin-C)

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13
Q

Factors that change contraction via changing Contractility: Cardiac glycosides

A

ie: digitalis - increases strength of contraction ONLY
positive inotropic effects

block Na/K pump, which conserves ATP
increases Na concentration inside therefore lowering gradient for Na to come in.
Decreases Na/Ca exchange, so Ca builds up inside
SR Ca content goes up, increasing contraction strength

BUT – overloading SR with Ca can result in DADs

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14
Q

Factors that change contraction via changing Contractility: Ca channel blockers

A

(Verapamil, Diltiazam, nifedipine) - increases Refractory period of slow response cells
negative inotropic effects on heart

Block Ca channels
Less Ca influx in heart
Less SR Ca content = decrease in contraction strength

good for treating arrhythmias bc is blocks slow Ca channel responses of AV node

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15
Q

Force-Frequency relationship - all has to do with time allotted for Ca handling

A

Tells us that HR and rhythm affects contraction force

Fast HR = less time for filling and Ca extrusion therefore more Ca retained in SR and contractions become stronger
(positive staircase effect)

Slow HR = more time for Ca handling/extrusion, therefore less Ca retained in the SR and contractions become less strong
(negative staircase effect)

16
Q

Force-Frequency relationship - Premature beat

A

A premature beat would UNEXPECTEDLY allow less time for Ca handling, so less Ca is uptaken into the SR and less contraction occurs

17
Q

Force-Frequency relationship - Post extrasystolic potentiation (the beat after a premature beat)

A

This beat is extra strong because there is now a lot of time for Ca handling and a lot of Ca makes it back into the SR so the contraction is much stronger

18
Q

Sign of Atrial fibrillation

A

1) very fast pulse
2) pulse varies, force in each beat is different
3) irregular irregular beats