Baroreceptor Mechanism and Reflex Heart Rate

Overview

1. The Baroreceptors (Sensors)

• Carotid sinus - at the bifurcation of the common carotid artery into internal and external carotid arteries. Responsive to both increases and decreases in arterial pressure.
• Aortic arch - primarily responsive to increases in arterial pressure.

• Changes in arterial pressure alter the stretch on the vessel wall.
• Stretch produces a receptor (generator) potential in the mechanoreceptor membrane.
• A depolarizing receptor potential increases action potential frequency in the afferent nerve; a hyperpolarizing potential decreases it.
• Increased Pa → increased stretch → increased firing rate in afferent nerves.
• Decreased Pa → decreased stretch → decreased firing rate.

2. Afferent Pathways

3. Central Integration: Brainstem Cardiovascular Centers

4. Integrated Reflex Response: Response to Increased Arterial Pressure (Step-by-Step)

1. Increased Pa → increased stretch on carotid sinus and aortic arch baroreceptors
2. Increased firing rate in CN IX (glossopharyngeal) and CN X (vagus) afferents
3. Signals arrive at the NTS; NTS detects Pa > set-point
4. NTS produces a coordinated response:
   • Increases parasympathetic outflow (via vagus) to the SA node → decreases heart rate
   • Decreases sympathetic outflow to the SA node (complements parasympathetic) → further decreases heart rate
   • Decreased sympathetic outflow to cardiac muscle → decreased contractility → decreased stroke volume
   • Together: decreased cardiac output → Pa falls
5. Decreased sympathetic outflow to arterioles → arteriolar vasodilation → decreased TPR → Pa falls further
6. Decreased sympathetic outflow to veins → venodilation → increased venous compliance → increased unstressed volume → decreased stressed volume → reduced venous return
7. Once Pa returns to set-point (~100 mmHg), baroreceptor firing and cardiovascular centers return to tonic baseline

• Costanzo Physiology 7th Edition, p. 171

5. Response to Decreased Arterial Pressure (e.g., Hemorrhage)

• Decreased Pa → decreased baroreceptor stretch → decreased afferent firing
• NTS detects Pa < set-point
• Decreased parasympathetic outflow + increased sympathetic outflow:
  • Heart rate increases
  • Contractility increases → cardiac output rises
  • Arteriolar vasoconstriction → increased TPR
  • Venoconstriction → decreased unstressed volume → increased venous return (Frank-Starling mechanism) → increased cardiac output

6. Heart Rate Specifically: Dual ANS Control

7. Clinical Modifications of the Reflex

• Chronic hypertension: Baroreceptors reset to a higher set-point - they no longer perceive elevated pressure as abnormal, so hypertension is maintained rather than corrected. - Costanzo Physiology 7th Edition, p. 170
• Reflex loses efficacy when Pa < 50 mmHg (severe shock). - Miller's Anesthesia 10th Edition, p. 1430
• Volatile anesthetics (particularly halothane) inhibit the heart rate component of the reflex.
• Ca²⁺-channel blockers, ACE inhibitors, phosphodiesterase inhibitors attenuate the reflex by direct peripheral vascular effects or CNS signaling interference.
• Bainbridge reflex counterbalance: At high circulating volumes, the Bainbridge reflex (atrial stretch → increased HR) opposes the baroreceptor reflex; at low volumes, the baroreceptor reflex dominates. - Medical Physiology (Boron & Boulpaep)

Summary Diagram of the Full Arc

↑ Arterial Pressure
       ↓
Baroreceptors (carotid sinus + aortic arch) — stretch ↑ → firing ↑
       ↓
CN IX / CN X → Nucleus Tractus Solitarius (medulla)
       ↓
   ┌──────────────────────────────────┐
   ↑ Parasympathetic               ↓ Sympathetic
   (cardiac decelerator)     (cardiac accelerator + vasoconstrictor)
       ↓                              ↓
   ↓ Heart rate (vagus/SA node)    ↓ HR, ↓ contractility, ↓ TPR, ↓ venous tone
       ↓
   ↓ Cardiac output + ↓ TPR → ↓ Pa → restored to set-point