Hypoxic pulmonary vasoconstriction (HPV) diverts blood away from poorly ventilated lung regions. The mechanism of HPV is unique because, unlike systemic vessels, pulmonary arteriolar smooth muscle:

• A Dilates in response to low O2 via nitric oxide release from the endothelium
• B Responds to low PO2 by releasing prostacyclin, causing paradoxical dilation
• C Constricts in response to low alveolar PO2 through inhibition of voltage-gated K+ channels (Kv channels), causing membrane depolarization and Ca2+ entry via L-type Ca2+ channels ✓
• D Constricts via sympathetic alpha-1 adrenergic stimulation in response to hypoxaemia

Explanation

In pulmonary vascular smooth muscle cells, low alveolar PO2 inhibits oxygen-sensitive voltage-gated K+ (Kv) channels. The resulting K+ channel closure leads to membrane depolarization, opening voltage-gated L-type Ca2+ channels, increasing intracellular Ca2+, and causing vasoconstriction. This is the opposite of systemic vessels (which dilate in hypoxia via K+ channel-mediated hyperpolarization). HPV is a local mechanism optimizing V/Q matching. In global hypoxia (e.g., high altitude), generalized HPV elevates pulmonary artery pressure, causing high-altitude pulmonary oedema.

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

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Written and medically reviewed by the StethoPrep medical team.