Effect of hypoxia on the contractile response to KCl, prostaglandin F2α, and hemoglobin

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Abstract
✓ The purpose of this experiment was to evaluate the effect of hypoxia on thein vitrocontractile responses of canine basilar artery to KCl, prostaglandin (PG) F2α, and hemoglobin. Hypoxia was induced by changing the bubbling gas mixture in the chamber from 95% O2/5% CO2to 95% N2/5% CO2. Hypoxia augmented the contractile response developed at 95% O2to 25 mM and 50 mM KCl, 3 × 10−7M and 10−5M PGF2α, and 10−6M hemoglobin. No significant alteration of the hypoxic augmentation in any preparation exposed to 25 mM KCl, 3 × 10−7M PGF2α, or 10−6M hemoglobin was observed with guanethidine (10−5M), prazosin (10−5M), methysergide (10−5M), or diphenhydramine (10−5M).Endothelial denudation did not affect hypoxic augmentation. Hypoxia did not cause any alteration of the contractile response to 10−6M PGF2αin Ca++-free media. Pretreatment with a calcium channel blocker, nicardipine, significantly inhibited the hypoxic potentiation of the contractile response to 25 mM KCl, 3 × 10−7M PGF2α, and 10−6M hemoglobin.These results suggest that hypoxia augments the contractile response to these agonists by a direct action on the smooth-muscle cells, facilitating the transmembrane influx of extracellular calcium. Hypoxia of smooth-muscle cells in the major cerebral arteries might be involved in the pathogenesis of vasospasm.
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