3. Old stuff
          3.2. Old physio stuff (around 2005)
              3.2.3. Physiology
                  3.2.3.2. Cardiovascular
                      3.2.3.2.4. Regulatory mechanisms
                          3.2.3.2.4.1. Regulation of heart rate
 3.2.3.2.4.1.1. ANS innervation of the heart 

ANS innervation of the heart

[Ref: BL8: chp4]

Parasympathetic pathway to heart

Via vagus nerve
* Originate in medulla oblongata

  • Right vagus nerve affect SA node predominantly
  • Left vagus nerve affect AV node predominantly

 

Vagal pathway

  • Neurons giving rise to vagal fibres are in:
    * Dorsal motor nucleus of the vagus, AND
    *Nucleus ambiguus
  • Innervation is to the heart only
  • Inhibited by neural input from NTS

[WG21:p608(fig31-8)]

Timing of vagal stimulation on heart

  • Brief in duration of action (nodes are rich in cholinesterase)
  • Very fast in onset
    * Because muscarinic receptors (M2) act via Gi protein which is coupled to a K+ channel

Effect of parasympathetic stimulation

[BL8:p88(fig4-4)]

Stimulates muscarinic acetylcholine receptors (M2)

--> Coupled with Gi protein

--> Inhibits adenylyl cyclase

--> Decrease cAMP

--> Decrease conductance of Ca2+

--> Decrease myocardial contractility

Also,

--> Gi protein is coupled to a K+ channel

--> Increased K+ conductance

--> Decreased RMP

--> Decrease HR (when acting on nodes)

Also,

  • ACh released from vagal endings can inhibit release of norepinephrine from nearby sympathetic nerve endings
    --> Reciprocal inhibition

Sympathetic pathway to heart

Originate in intermediolateral column of upper 5-6 thoracic and lower 1 or 2 cervical segements of the spinal cord

Timing of sympathetic stimulation on heart

  • Slower onset than vagal (mediated by cAMP)
  • Effects decay very gradually

Effect of catecholamines

Stimulates beta-1 receptor

--> via Gs protein

--> Activate adenylyl cyclase

--> Increase cAMP

--> Activate protein kinase A

--> Phosphorylation of Ca2+ channels on membrane

--> Channels open for longer

--> Greater Ca2+ influx

--> Greater contractility

Also,

Protein kinase A

--> Phosphorylation of phospholamban

--> Stimulation of calcium pump on SR

--> Increased active transport of Ca2+ to SR

--> Faster relaxation

[BL8:p105]

Plus,

Protein kinase A

--> Phosphorylation of Troponin I

--> Inhibition of Ca2+ binding by Troponin C

--> Relaxation

--> Faster relaxation

NB:

  • Catecholamines also increase sensitivity of myofilaments to Ca2+

Normal heart rate

At rest, there is a certain level of vagal tone at rest.

When vagus is cut, HR increase from 70 to 150-180 because sympathetic tone is unopposed.

 

Custom fields
3 :20050816