Peripheral chemoreceptors (carotid bodies) are primarily stimulated by which mechanism under sustained hypoxia?

• A Low CaO₂ (oxygen content): anemia equally stimulates carotid bodies as does low PaO₂
• B Reduced pH detected by extracellular acid-sensing ion channels in glomus cells
• C Low PaO₂ directly (not CaO₂): inhibition of K⁺ channels in type I glomus cells causes depolarization and neurotransmitter release ✓
• D Hypercapnia alone is the primary stimulus; hypoxia is a secondary modulator

Explanation

Carotid body type I (glomus) cells are uniquely sensitive to low arterial PO₂, not oxygen content per se — this is why anemia (low CaO₂ but normal PaO₂) does not strongly stimulate carotid chemoreceptors. Hypoxia inhibits O₂-sensitive K⁺ channels (proposed TASK and BK channels) in glomus cells, causing depolarization, Ca²⁺ entry, and release of neurotransmitters (dopamine, substance P, acetylcholine) onto carotid sinus nerve (CN IX) afferents. While CO₂/pH are also stimuli, the O₂-sensing K⁺ channel mechanism is unique to peripheral chemoreceptors — central chemoreceptors are insensitive to hypoxia.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.