Hypoxic pulmonary vasoconstriction (HPV) is a unique reflex diverting blood from poorly ventilated lung regions. Which mediator or mechanism has been most established as the cellular sensor and effector of HPV?
- A Hypoxia inhibits voltage-gated K+ channels (Kv) in pulmonary artery smooth muscle cells, causing depolarization, Ca2+ influx, and vasoconstriction ✓
- B Pulmonary endothelium releases endothelin-1 in response to hypoxia, directly contracting VSMCs
- C Alveolar hypoxia stimulates type II pneumocytes to release leukotriene B4, which contracts pulmonary arterioles
- D Hypoxia activates HIF-1α in endothelium, immediately upregulating eNOS and causing paradoxical vasoconstriction
Explanation
HPV is intrinsic to pulmonary artery smooth muscle cells (PASMCs) and does not require neural or endothelial input for initiation. The primary mechanism involves oxygen sensing in the mitochondria of PASMCs: hypoxia increases reactive oxygen species (or decreases them, debated) and redox signals inhibit Kv (voltage-gated K+) channels on the plasma membrane. K+ channel inhibition depolarises the PASMC, opens voltage-dependent L-type Ca2+ channels, raises intracellular Ca2+, and triggers actin-myosin cross-bridging and vasoconstriction. This redirects blood to better-ventilated alveoli, optimising V/Q matching.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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