Abstract

1. The 60 mM K +, 152 mM K +, Na-deficient medium and oubain-induced contractions of aorta were not so affected by severe hypoxia. 2. The 60 mM K +, 152 mM K +, Na +-deficient medium-induced responses were greatly reduced by deprivation of external Ca 2+ in normoxia. 3. As the concentration of epinephrine increased, the remaining tensions which were expressed as a percentage of the original tensions became progressively greater in hypoxic condition. 4. The percentage of resistant components of the norepinephrine-induced contraction by the lower concentration was further reduced in Ca 2+-free medium by severe hypoxic condition. 5. The tensions under normoxia and lactate release under severe hypoxia induced by 60 mM K + or 2.5 × 10 −6 M epinephrine were of the same extent. 6. In conclusion, the inhibition of aortic response to epinephrine with severe hypoxia could not solely be explained by depression of the oxygen supply into the oxidative metabolism. Severe hypoxia did not affect Ca 2+ influx through voltage-operated Ca 2+ channels, but reduced both receptor-operated Ca 2+ influx and intracellular Ca 2+ release in the aorta.

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