• long preganglionic fibers
  • releases ACh to act on nicotinic receptors
• short postganglionic fibers
  • release ACh to act on muscarinc receptors on heart

• short pre-ganglionic fibers
  • releases ACh to act on nicotinic receptors
• long post-ganglionic fibers
  • releases norepinepherine to act on beta one receptors

Effect of hexamethonium on ANS

• once muscarinic receptors stimulated by ACh, they activate potassium channels
  • hyperpolarize cell
  • decrease rate of depolarization

This all leads to pacemaker cells firing at lower frequency.

The two nuclei in the medulla responsible for tonic parasympathetic stimulation of heart

nucleus ambiguus (predominant)

dorsal motor nucleus of the vagus

• once norepinepherine activates beta 1 receptors, stimulates phosphorylation of I(f) channel
  • increases influx of sodium and calcium through the channels
  • decreases threshold for voltage gated calcium channels

Increase rate of depolarization and increase excitability.

Area of brain responsible for sympathetic activity of heart and bv

vasoconstriction

• sparse parasymp. innervation
  • so if you gave somebody a muscarinic/cholinergic agonist, there would be vasodilation
  • BUT, if you gave somebody an muscarinic antagonist, there would not be much affect on blood vessel diameter

• aorta
• common carotid A.
• vena cava
• jugular V.

Composition of afferent fibers in baroR

• located within carotid sinus 
  • A fibers- myelinated (fire first)
  • C fibers- unmyelinated (fire only at higher pressures)

It resets its "normal pressure" firing level, so it cannot fight the new HTN. This also complicates treatment.

Neuronal pathway for baroR's when blood pressure is elevated

1. senses high pressure, begins to fire (A first, than C at much higher pressure)
2. afferent fibers conduct along CN IX and X
3. stimulates nucleus tractus solitarious via stimulation of NMDA receptors with Glu
   1. stimulate preganglionic parasympathetics in the nucleus ambiguus and dorsal motor nucleus of vagus N.
   2. increased inhibition of the preganglionic sympathetic neurons in ventrolateral medulla (inhibit β1 R's)

• inspiration inhibits parasympathetic preganglionic cardiac neurons, leading to an increase in heart beat during inspiration
• benefit- improve ventilation to perfusion ratios

1. increases intrathroacic pressure
2. decreases venous return to the heart
3. leads to reduced CO and reduced bp
4. decrease in baroR discharge
   1. reduced activation of parasymp. sys.
   2. reduced inhibition of symp. sys.
5. increased HR, contractility, vasoconstriction

1. pressure in carotid sinus decrease due to effect of gravity
2. this leads to decrease baroR discharge

Upon prolonged standing, there can be pooling in the lower extremities.

• initial reaction
  • increase sympathetic and decrease parasymp. to restore bp to normal levels
• severe situations- decompensatory phase
  • reflex bradycardia and decrease vascular resistance, leading to decrease bp
  • how- activation of sensory vagal afferents from heart

1. there is a huge decrease in cerebral blood flow
2. cerebral chemoreceptors activated
3. increase in symp. activity of heart and peripheral arterioles, increase arterial pressure to extremely high levels

1. initial response- increase in HR via central command (can happen even before exercise)
2. second phase
   1. accumulation of lactic acid leads to local vasodilation within exercising skel. musc.
   2. this will evolke baroreflex mediated decreases in parasymp. and increases in symp. activity
   3. leads to bp restored, CO increases, and vasoconstriction in other regions (non-exercising regions)
3. Thrid phase
   1. if exercise intese, stimulate adrenal medulla to release epinepherine
   2. stimulates beta 2 receptors to cause vasodilation

1. stimulation of trigeminal nerve, more specifically the nasotrigeminal sensory nerve fibers
2. increase parasymp. activity, leads to decrease HR

Usually seen in infants and men more significant.