Baroreceptors

Describe the function of baroreceptors and to relate this knowledge to common clinical situations.

Baroreceptors are stretch receptors which monitor changes in arterial pressure. Arterial pressure is monitored by receptors in the:

• Aortic arch
  • Innervated by CNX
• Carotid sinus
  Small dilation of the ICA at the level of the bifurcation.
  • Innervated by CNIX
  • Remember the carotid sinus is a baroreceptor, the carotid body is a chemoreceptor

Low-pressure stretch receptors:

• Respond to increased venous return
• Are inhibited by positive pressure ventilation
• Act by stretch and typically described as volume receptors
• Are located in the:
  • Atrial walls
  • SVC and IVC
  • Pulmonary circulation

Baroreceptor Control

Afferent fibres from CNIX and CNX travel to the NTS in the medulla. Effector neurons from the RVLM are GABAergic and therefore inhibitory, i.e. increased baroreceptor discharge reduces tonic sympathetic tone and increases vagal tone.

Increased baroreceptor activity therefore results in:

• Arterial and venous vasodilation
• Hypotension
• Bradycardia
• Decreased cardiac output
• Decreased respiratory rate

Conversely, increased activity of low-pressure stretch receptors results in an increase rather than a decrease in heart rate.

Baroreceptor Activity

Baroreceptors are:

• More sensitive to pulsatile pressure than constant pressure
  A decrease in pulse pressure without a change in MAP will decrease baroreceptor firing.
• Active throughout the cardiac cycle
  Rapid compensatory responses are vital in the short-term control of blood pressure, e.g. with posture.
• Active over the range from 50mmHg to 200mmHg

• This curve is left-shifted in children and neonates, and right-shifted in chronic hypertension, though this is reversible

Hormonal control

Activation of atrial/ventricular stretch receptors stimulates ANP/BNP release respectively, which act to reduce blood pressure in the following ways:

• Increased GFR
  Act to constrict the efferent arteriole and dilates of the afferent arteriole. This subsequently inhibits renin secretion through increased hydrostatic pressure at the JGA and increased Na⁺ and Cl^- delivery to the macula densa.
• Decreased aldosterone
  Via inhibition of aldosterone secretion.
• Vasodilation
  Causes vasodilation of peripheral smooth muscle.

References

1. Barrett KE, Barman SM, Boitano S, Brooks HL. Ganong's Review of Medical Physiology. 24th Ed. McGraw Hill. 2012.
2. CICM September/November 2014
3. ANZCA July/August 2000