Hypoxia inhibits calcium influx in rabbit basilar and carotid arteries

We examined the hypothesis that hypoxia inhibits Ca²⁺ influx in isolated rabbit common carotid, internal carotid, and basilar arteries. In arteries mounted for measurement of isometric tension and exposed to 122 mM K⁺ in Ca²⁺-free Krebs, cumulative addition of Ca²⁺ produced Ca²⁺-force relations that were right-shifted by hypoxia (PO₂ ~ 15 Torr) with no decrease in maximum force attained. In arteries precontracted with 122 mM K⁺, exposure to hypoxia produced relaxations whose rates and magnitudes were enhanced by reductions in bath Ca²⁺ from 8.0 to 0.8 mM. Using an ethylene glycol-bis(β-aminoethyl ether)-N,N,N',N'- tetraacetic acid method for 3-min ⁴⁵Ca influx measurements, modified for use in rabbit basilar and carotid arteries, we found that resting levels of Ca²⁺ influx (μmol·min^-1·kg dry wt^-1) were significantly higher in basilar (67 ± 1, n = 10) than in internal carotid (27 ± 1, n = 12) or common carotid (33 ± 1, n = 12) arteries. K⁺ stimulation increased Ca²⁺ influx more than two-fold compared with control in all three artery types, and hypoxia inhibited this increase by 74% in basilar, 49% in internal carotid, and 33% in common carotid arteries. Exposure to 10 μM serotonin and 100 μM uridine 5'-triphosphate (UTP) also increased Ca²⁺ influx, but these increases were less than observed during K⁺ contractions and averaged 10 (basilar), 31 (internal carotid), and 82% (common carotid) above control. Hypoxia completely inhibited serotonin- and/or UTP-induced increases in Ca²⁺ influx in basilar and internal carotid segments and inhibited 47% of this increase in the common carotid segments. We conclude that hypoxic inhibition of Ca²⁺ influx is an important component of the overall response to hypoxia and that the mechanism of this effect appears dependent on the method of contraction.