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

I_K-Ach is increased by Ach

I_CaL type: is increased by NE and decreased by Ach

I_f is increased by NE and decreased by Ach

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

Parasympathetic: Decreased I_f slows the rate of phase 4 depolarization, decreased I_Ca make TP more positive, increased I_K-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.

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 I_Ca and I_f would increase HR

Sympathetic: increased I_Ca 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 I_K-Ach slows CV by opposing I_Ca, decreased I_Ca decreases dV/dt and therefore CV, together thest prolong the ARP and ERP

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

1) Increased I_Ca 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

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

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

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.

G_s stimulates adenylate cyclase and G_{i or K} inhibit adenylate cyclase.  G proteins can also have direct effects on ion channels.

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

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

G_s has direct effect to stimulate adenylate cyclase and Ca channels