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Flashcards in Cardiac Excitation Deck (43)
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How do we know there is tonic parasympathetic activity in the heart?

administration of atropine (cholinergic M2 receptor antagonist) increases the heart rate up to 120 bpm at maximal dosage


How do we know there is tonic sympathetic activity in the heart?

If propranolol (a beta adrenergic antagonist) is given, heart rate drops to about 50 beats/min, indicating modest tonic adrenergic activity.


How does contraction of heart muscle occur?

Intracellular Ca is the critical activator of cardiac muscle contraction similar to that in all other muscle types;

Ca channels are activated in the plateau phase: phase 2; shortly after intracellular Ca reaches a peak concentration, contraction begins; subsequently, as intracellular Ca is decreased, contraction returns to baseline


What activates Ca channels to initiate contraction? Is Ca entry enough to initiate contraction?

Depolarization activates Ca channels; however, entry of Ca via channels is insufficient to activate the contractile machinery by itself


What else does contraction require?

Contraction requires supplemental Ca release from an intracellular Ca reservoir, the SR (sarcoplasmic reticulum). Faster and larger Ca influx cause more SR Ca release

Contraction is a property that is graded based on the intracellular Ca concentration


What is the other major factor controlling contractility?

fiber length- in turn related to preload volume which stretches fibers.


How does influx of ca release more Ca from the SR?

Ca binding to RyR (ryanodine receptor) in SR releases sufficient Ca to cause myofilament activation.


How is Ca removed from myocytes after contraction?

Ca is removed via the cell membrane pumps and exchangers (3Na in for 1Ca out- no ATP needed here- but can work in other direction- BAD), the SR and the mitochondria.

It should be noted however that mitochondria (beat to beat) are the least important in this regard although they may play a role in the long-term, as Ca reservoirs.


How do catecholamines (Epi or Nor) act in the heart?

They bind to Beta adrenergic receptors, which associates with a G protein called Gs which activates adenylate cyclase to produce cAMP which releases PKA from its regulator. PKA then phosphorylates the calcium channel activating it (more Ca in) and the RYR receptor on the SR causing increased Ca release during the response

Ca is taken back up in the SR via an ATP dependent pump (with a subunit called phospholamban which when phosphorylated via PKA from catecholamine binding actually inhibits the pump)


What is the Frank Starling mechanism?

increased sarcomere length results in increased active tension, up to a physiological limit (the maximum of the active tension curve). I.e. stretching the ventricles= increased tension and stroke volume


T or F. Up to a physiological limit, the normal heart will pump out any end diastolic volume (EDV) and reach the same end systolic volume (ESV), thus causing increased stroke volume.

T. Linear relationship

The greater the EDV, the greater the SV


How does an increase in length translate into increased cardiac force generation?

Increasing the length of the fibers makes the fibers more sensitive to Ca (up to a point where it plateaus) and a slow response to stretch exists involving activation of calcium channels by stretch (so more Ca comes in and the filaments become more sensitive to it)

whereas the inverse is true for shortening


How does ACh act in the heart?

ACh binds to an M2 receptor (with Gi) and inhibits AC and cAMP production which prevents PKA release from its regulator.