Every other vascular bed in the body dilates when starved of oxygen. The pulmonary circulation does the opposite: falling alveolar O₂ closes oxygen-sensitive K⁺ channels in arteriole smooth muscle, depolarizing the cell and driving Ca²⁺ influx and constriction — routing blood away from poorly ventilated alveoli toward better-oxygenated ones. Each segment's constriction is computed from a real gain formula:
constriction = clamp( gain × (100 − O2) / 100, 0, 0.85 )
vessel radius factor r = 1 − constriction × 0.82
flow weight = 1 − constriction (Poiseuille: resistance ∝ 1/r⁴)
Blood-flow particles pick a destination segment with probability proportional to its flow weight, so a fully constricted segment still receives a trickle (vessels never fully close) while open segments receive proportionally more. When only one segment is hypoxic (a blocked bronchus), this is a protective local adjustment. When the whole lung is hypoxic (e.g. high altitude), every arteriole constricts together, and the relative pulmonary vascular resistance index — the mean of 1/r⁴ across all segments — rises instead of blood simply being redirected, which is the mechanism behind altitude-related pulmonary hypertension.