Pulmonary Receptors

Introduction

1. Slowly Adapting Pulmonary Stretch Receptors (SARs / PSRs)
2. Rapidly Adapting Receptors (RARs) - "Irritant Receptors"
3. C-Fiber Receptors (J Receptors / Juxtacapillary Receptors)

1. Slowly Adapting Pulmonary Stretch Receptors (SARs)

Location

• Located in the smooth muscle of the tracheobronchial tree, from the extrathoracic trachea down through the intrapulmonary bronchi.

Fiber type

• Afferent signals travel via myelinated vagal fibers - hence rapid conduction.

Stimulus

• Activated by lung inflation (mechanical stretch of airway walls).
• Discharge increases with lung inflation and decays very slowly over time (hence "slowly adapting").
• Not significantly stimulated by chemical stimuli (exception: hypocapnia can activate them).

Reflex - The Hering-Breuer Reflex

• Sustained lung inflation activates SARs → vagal afferents signal the medulla → inspiratory activity is terminated (phrenic motor neuron output is inhibited) → expiration begins.
• This prevents over-inflation of the lungs and helps regulate tidal volume.
• It also increases respiratory frequency by shortening inspiration, maintaining constant alveolar ventilation.

• Marked deflation of the lung → decreases the duration of expiration → promotes the next inspiration.

Clinical Significance

• In human adults, this reflex operates mainly above tidal volume range - it is particularly active in pathological over-inflation and in newborn infants where it helps regulate normal breathing.
• Feedback from SARs may also help the medulla select the optimal combination of tidal volume and respiratory frequency to minimize work of breathing.

2. Rapidly Adapting Receptors (RARs) - "Irritant Receptors"

Location

• Located throughout the tracheobronchial tree, primarily in the epithelial and submucosal layers of the larger airways (trachea and large bronchi).

Fiber type

• Afferent signals travel via myelinated vagal fibers (same as SARs but different receptors).

Stimulus

• Respond to sudden, sustained lung inflation with a rapid increase in firing rate that decreases to 20% or less of initial rate within 1 second (hence "rapidly adapting").
• Also stimulated by rapid lung deflation.
• Unlike SARs, RARs are highly sensitive to a wide range of chemical irritants:
  • Histamine, serotonin, prostaglandins, bradykinin
  • Ammonia, cigarette smoke, ether
  • Dust and particulates
  • Mucus, edema fluid
• This chemical sensitivity gave them the name "irritant receptors."
• They also increase firing as rate of airflow increases.

Reflexes Mediated

Clinical Significance

• These receptors detect pathophysiological processes in the airway: chemical irritation, mucosal congestion, inflammation, and edema.
• They drive the cough reflex - a critical airway defense mechanism.
• They contribute to bronchoconstriction seen in asthma and anaphylaxis.
• Laryngeal narrowing and cough triggered by inhaled irritants are primarily RAR-mediated.

3. C-Fiber Receptors (J Receptors / Juxtacapillary Receptors)

Location

• Nerve endings of unmyelinated C fibers situated in alveolar walls and conducting airways, close to pulmonary capillaries - hence the name "juxtacapillary (J) receptors" (proposed by Paintal).
• Two subgroups:
  • Pulmonary C fibers - near pulmonary capillaries in alveolar walls
  • Bronchial C fibers - near bronchial circulation in the airways

Fiber type

• Unmyelinated (C fibers) - slow conduction velocity.
• Travel centrally via the vagus nerve.

Stimulus

• Stimulated by hyperinflation of the lung.
• Also stimulated by increases in pulmonary vascular pressure and capillary pressure (pulmonary vascular congestion, pulmonary edema).
• Respond to exogenously and endogenously released chemicals:
  • Capsaicin (classical J receptor stimulant - used experimentally)
  • Phenyl diguanide
  • Bradykinin, serotonin, prostaglandins
  • Substances released during pulmonary embolism and congestion

Reflex - Pulmonary Chemoreflex (Bezold-Jarisch-like reflex)

1. Apnea (brief cessation of breathing)
2. Followed by rapid, shallow breathing
3. Bradycardia
4. Hypotension (fall in blood pressure)
5. Bronchoconstriction
6. Increased mucus secretion

C-Fiber Triad

• Rapid and shallow breathing
• Bronchoconstriction
• Increased mucus secretion into airways

Clinical Significance

• Pulmonary edema: J receptors are stimulated by elevated pulmonary capillary pressure → rapid, shallow breathing (tachypnea) of left heart failure is partly J-receptor mediated.
• Pulmonary embolism: J receptors activated by released endogenous substances → reflex tachypnea.
• Exercise: Uncomfortable sensations from J receptor activation may contribute to the feeling of dyspnea and fatigue during intense exercise.
• Dyspnea in lung disease: Atelectasis, congestion, and inflammation all stimulate C fibers.

Comparison Table

Additional Receptors

Chest Wall and Respiratory Muscle Receptors

• Muscle spindles in intercostal muscles and the diaphragm detect changes in thoracic cage volume.
• Joint receptors in costovertebral joints and tendon organs in respiratory muscles project centrally via spinal nerves (not vagus).
• These are important during exercise, posture change, and in pathological conditions with decreased lung or chest compliance.
• Input from proprioceptors in muscles, tendons, and joints stimulates inspiratory neurons - this helps increase ventilation during exercise.

Nasopharyngeal and Upper Airway Receptors

• Afferent signals from the upper airways travel via CN IX (glossopharyngeal nerve).
• Stimulation produces cough, sneeze, and bronchoconstriction.

Afferent Pathway Summary

Clinical Correlations

Sources

• Ganong's Review of Medical Physiology, 26th ed., Ch. 36 - "Responses Mediated by Receptors in the Airways & Lungs"
• Medical Physiology (Boron & Boulpaep) - "Stretch and Chemical/Irritant Receptors in the Airways and Lung Parenchyma"
• Fishman's Pulmonary Diseases and Disorders - "Mechanoreceptors"
• Murray & Nadel's Textbook of Respiratory Medicine - "Controller Feedback"