Vasomotor centre

[Ref: WG21:chp31]

• In medulla oblongata
• Control of BP via vascular tone

See figure 31-7 [WG21:p607]

Pathway

Cell bodies

... of neurons mediating sympathetic discharge to CVS

Located near the pial surface of the medulla in the rostral ventrolateral medulla (RVLM).

Axons

Axons travel dorsally and medially, then descend in the lateral column of the spinal cord

Projection

Project to the sympathetic preganglionic neurons in the intermediolateral gray column (IML) of the spinal cord

Preganglionic neurons

Preganglionic neurons then innervate

• Adrenal medulla directly, OR
• Synapse in ganglion
  * Neurotransmitter: Ach

Postganglionic sympathetic neurons then innervate the heart and blood vessels
* Neurotransmitter: NE

NB:

• Contains PNMT (converts NE to E)
• But the excitatory neurotransmitter (in IML) is glutamate, not epinephrine.

 

Factors affecting vasomotor centre activity

Summary

A. Directly stimulated by

• CO2
• Hypoxia

(Presumably directly on RVLM)

B. Excitatory inputs

• From cortex via hypothalamus
• From pain patheways
• From muscles
• From peripheral and central chemoreceptors

C. Inhibitory inputs

• From cortex via hypothalamus
• From lungs
• From carotid, aortic, and cardiopulmonary baroreceptors

D. Other factors

• Stimulation of chemoreceptors
• ICP

Inflation of lungs

(via vagal afferent)

--> Vasodilation and decreased BP

Pain

--> Increase BP via reticular formation[WG21:p606]

But prolonged pain

--> Vasodilation and fainting

Somatosympathetic reflex

... refers to stimulation of somatic afferent nerve causing pressor response

Probably via C1 neurons in the RVLM

Chemoreceptor

[WG21:p612]

Stimulation of peripheral chemoreceptor (e.g. in stagnant hypoxia due to hemorrhage) leads to

• Bradycardia
  * ??Transient [BL8:p192, fig 8-11]
• Vasoconstriction
• Overall increase in BP

Stimulation of central chemoreceptor (e.g. by increased PaCO2, decrease pH)
--> Vasoconstriction

[BL8:p192]

NB:

• Effect is small compared to direct effect of hypoxia and hypercapnia on vasomotor area.
• Potentiate vasoconstriction in haemorrhage
• But if both baroreceptors and chemoreceptors are stimulated, baroreceptor predominate
  [BL8:p192]

Direct stimulation of vasomotor area

Hypoxia

Direct effect of hypoxia is small (compared with effects of hypercapnia)

• Moderate hypoxia stimulates vasomotor activity
• Very severe hypoxia depresses vasomotor activity

Hypercapnia

Increase in PaCO2 stimulates vasomotor area
--> Vasoconstriction

But,

Increase in PaCO2 directly causes peripheral vasodilation
* Especially in skin and brain

Overall,

--> Slow rise in BP

ICP and bradycardia

When ICP is increased
--> Impaired blood perfusion
--> Hypoxia and hypercapnia in vasomotor area
--> Increase in BP (Cushing reflex)
--> Reflex decrease in HR (via baroreceptors)

Thus, increased ICP is characterised by bradycardia

Respiration also slowed [WG21:p621]

Sympathetic vasodilator system

[WG21: p613]

Originates in cerebral cortex

--> Relays in hypothalamus and mesencephalon

--> Passes through (without synapsing) IML gray column of spinal cord

--> Synapse with postganglionic cholinergic neurons to blood vessels

• Produces vasodilation in skeletal muscles
  * Predominant factor in skeletal muscles during exercise is still local metabolite
• Associated with decrease in muscle O2 consumption (not increase)
• Role in human is UNCERTAIN
• May be responsible for fainting
• May be responsible for vasodilation at the start of exercise

Other notes