Neural control of the CVS

20 important questions on Neural control of the CVS

Which sensors excist that control the circulation?

  • Baroreceptors = blood pressure
  • Volume receptors = blood volume (low pressure baroreceptors)
  • Osmoreceptors = plasma osmolarity
  • Chemoreceptors = blood chemistry (pO2, pCO2, pH)  

The vascular resistance is controlled by a large number of influences, namely:

Extrinsic influences:
  • Neural (autonomic nerves)
  • Humoral (circulating hormones)
=> also influence heart rate, blood volume etc.

Intrinsic influences:
  • Tissue metabolites
  • local hormones
  • Myogenic
  • Endothelial factors

Which neurotransmitters are important for neural control of the vascular system?

Norepinephrine (sympathetic) and acetylcholine (parasympathetic)
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Where does Acetylcholine bind to?

Muscarine receptor (M2), which induces vasodilation in blood vessels and decreases inotropy, chronotropy and dromotropy in the heart.

chronotropy = heart rate
dromotropy = conduction velocity
inotropy = contractility

To which receptors does norepinephrine bind to?

ß-receptors (ß1 and ß2)
Alpha receptors (alpha1 and alpha2)

=> on the heart is particularly binds to ß1 receptors and to a lesser extend to the ß2 and alpha1 receptor => increase of inotropy, chronotropy and dromotropy

=> on blood vessels it particularly binds to alpha 1 receptors and to a lesser extend to alpha2 and ß2, the alpha receptors cause vasoconstriction and the beta receptor vasodilation

=> feedback loop regulates the release of NE, ACh inhibits the release of NE

What is the effect of muscarine receptors on the heart?

Decrease of inotropy, chronotropy and dromotropy

-> by ACh

What also influences the heart rate, besides neural and hormonal control?

Body temperature, +7 beats per minute per degree
Central venous/right atrial pressure, +6% per mmHg

What is the cascade that happens after norepinephrine activates the ß receptor?

GPCR: adenylate cyclase converts ATP -> cAMP. Which stimulates the inward currents If and Ica, thus increasing the pace maker

What is the cascade after stimulation of ACh?

Stimulates Gi (muscarine receptor), so it inhibits adenylate cyclase, and thus the stimulation of the inward currents If and Ica. Furthermore, it stimulates the K+ channels, so increasing the outward current Ik and decreasing the pacemaker rate

What is the effect of beta blockers?

They blok the beta receptor, thus inhibits sympathetic influence -> lowers the heart rate

=> propranolol

What is the effect of a muscarinic receptor antagonist?

Inhibits parasympathetic influence -> increases the heart rate

=> atropine

How is the brain activated to raise/lower the heart rate?

- work (using muscles)
- thinking
- feel (temperature, pain)
- breathing
- blood pressure

Where are the baroreceptors located?

In the aortic arch
in the glossopharyngeal nerve (9th cranial nerve)

Which center in the brain computes al the somatosensory information?

Nucleus tractus solitarii

What is the indirect way for regulating the SA node?

Via the adrenal medulla (catecholamines)

What is the effect of baroreceptor firing?

Inhibits sympathetic outflow and stimulates parasympathetic outflow

What is baroreceptor resetting?

Baroreceptors adjust within 10-30 minutes to the current blood pressure

What is the baroreceptor sensitivity?

Change in firing rate per mmHg blood pressure change, is largest at the predominating blood pressure

What are the predominant type of receptors in skletal muscle and in coronary and bronchial circulations?

Skeletal = alpha (vasoconstriction)
Coronary and bronchial circulation = ß2 (vasodilation)

What is the difference between epinephrine and norepinephrine?

Epinephrine (adrenalin), is produced by the adrenal glands under sympathetic stimulation. It acts differently from norepinephrine (which is produced at sympathetic nerve terminals).
Epinephrine binds preferably to ß2 receptors, while norepinephrine binds preferably to alpha1 receptors. Hence, in skeletal muscle, a low plasma concentration of epinephrine gives vasodilation due to the ß2 effect. But eventually (at higher concentration) it also binds to alpha receptors and the vasoconstriction wins)

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