Shared Flashcard Set


Autonomic Regulation of Cardiac Function
VCU PHIS 501 October 7, 2010

Additional Physiology Flashcards




Basics of Autonomic Innervation and Effects

Parasympathetic: vagus nerve, supraventricular, Ach acts on M2 receptor in heart, blocked by atropine


Sympathetic: superior cervical ganglion, NE acts on β1, blocked by nonselective propranolol


Effects are usually antagonist.  At rest, heart in under parasympathetic control. 


HR= chronotropic

Conduction Velocity= dromotropic

Contractility= inotropic

What currents do the autonomics effect?

IK-Ach is increased by Ach

ICaL type: is increased by NE and decreased by Ach

If is increased by NE and decreased by Ach

Chronotropic effects at the SA node

Sympathetic: increased If increases the rate of depolarization and increased ICa makes TP more negative- together these increase the HR because there is less time spent in phase 4


Parasympathetic: Decreased If slows the rate of phase 4 depolarization, decreased ICa make TP more positive, increased IK-Ach makes MDP more negative- together these decrease the HR by increasing time spent in phase 4


Since, there are three ways the parasympathetic system effect the HR, at rest the heart is under parasympathetic control.  Parasympathetic withdrawal would increase HR.



Chronotropic Effects at the AV node and HIS PKJ system

AVN- essentially the same as SAN, strong SNS stimulation or PNS withdrawal may make automaticity noticable


HIS-PKJ: only effected by SNS since it is not supraventricular, so increase in ICa and If would increase HR

Dromotropic Effects at the AV node

Sympathetic: increased ICa so increased dV/Dt so more rapid conduction velocity.  This increase also decreases the lenght of the refractory periods since there are more Ca channels.  Decreased ERP means decreased AV delay- AVN can conduct AP at higher heart rates


Parasympathetic: increased IK-Ach slows CV by opposing ICa, decreased ICa decreases dV/dt and therefore CV, together thest prolong the ARP and ERP



Dromotropic Effect in the atrium
Not physiologically important, but parasympathetic would increase conduction velocity because the increased IK-Ach would make the resting membrane potential more negative and therefore more sodium channels would be closed.
Sympathetic Inotropic Effects

Positive inotrope on both the atria and ventricle: increased peak tension, rate of tension development, rate of relaxation, and decreased twitch duration


1) Increased ICa results in a greater triger and greater filling of SR stores- greater SR stores means more forceful contraction

2) Faster relaxation due to increased rate of Ca accumulation caused by phosphorylation of phospholamban and decreased affinity for TnC and Ca

Parasympathetic Inotropic Effects

Negative in the atria, but the ventricle is not usually effected (only in presence of high sympathetic tone)


Ach decreases atrial contractility by increasing IK-Ach which decreased APD and therefore Ca entry into the cell and therefore contractility.  At high doses it directly decreases Ca by decreasing ICa

Basics of G-proteins

G proteins are heterotrimers which contain the alpha, beta, and gamma subunits- specificity is built into subunits (distinct subunits)


The alpha units bind GTP/GDP


Binding of a ligand activates the G-protein and the beta/gamma units dissociate from the GTP-bound alpha unit.  Both pieces remain in the membrane and one or both go to target protein.


G proteins are deactivated when GTP is dephosphorylized to GDP which then dissociates and a new GTP binds the alpha unit so it is able to be activated.


Gs stimulates adenylate cyclase and Gi or K inhibit adenylate cyclase.  G proteins can also have direct effects on ion channels.

β1 receptor activation

Gs couples the β1 receptor to adenylate cyclase which converts ATP to cAMP. cAMP activates PKA which phosphorylates many target proteins. 


PKA phosphorylation targets- Increases ICa stimulation, phopholambam (increases Ca uptake into SR), troponin (decreases the Ca sensitivity of the myofilaments)


Gs has direct effect to stimulate adenylate cyclase and Ca channels

M2 Receptor Activation
Gk/i couples the receptor to adenylate cyclase, but this receptor inhibits adenylate cyclase.  So, it reduces the amount of cAMP and therefore PKA.  This receptor directly activates K channels. (IK-Ach)
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