Effects of hypoxia on calcium fluxes and force development in the neonatal rat atrium

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Abstract
The effects of hypoxia on 45calcium fluxes and force development were studied in the resting and stimulated (high potassium/low sodium solutions or Bay K 8644) neonatal rat atrium. Under normoxic conditions, high potassium (100 mmol .cntdot. litre-1)/low sodium Tyrode solution and Bay K 8644 (2.5 .times. 10-5 mol .cntdot. litre-1) significantly increased calcium uptake above that measured in normal Tyrode solution. High potassium/low sodium Tyrode solution elicited a sustained tonic contracture. Bay K 8644 did not increase resting tension but induced spontaneous phasic contractions in some preparations. Hypoxia failed significantly to alter resting calcium uptake but partially inhibited (50-99%) the high potassium/low sodium and Bay K 8644 induced calcium uptake (that is, the calcium uptake above that measured in normal Tyrode solution). The magnitude of the high potassium/low sodium induced contracture was increased by hypoxia (15 min). Bay K 8644 had no effect on resting tension (in five out of six experiments) after 15 min of hypoxia. Acidosis failed to affect resting (with the exception of the 210 min time point), high potassium/low sodium induced, and Bay K 8644 induced calcium uptakes and had little effect on the high potassium/low sodium induced contracture. It is hypothesised that hypoxia reduces the cells'' ability to regulate calcium. Furthermore, it appears that hypoxia''s effects on calcium fluxes and the high potassium induced contracture involve other mechanisms besides the associated acidosis.