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Hypoxia is suggested to increase intracellular Ca2+, thereby affecting cellular functions. If this is the case, the effect would be modified by other treatments which also elevate intracellular levels of Ca2+. To test this possibility, in mouse diaphragm preparations, the effects of hypoxia were examined on twitch potentiations after application of neural conditioning pulses which are considered to elevate intracellular Ca2+. The effects were compared with those of 2,4-dinitrophenol (DNP) and ouabain. Hypoxia increased the tension of twitches elicited directly or neurally with 0.1 or 0.5 Hz pulses at 36 degrees C but not at 24 degrees C. Paired pulses to the nerve induced a complex response profile in which the amplitude of the second twitch was enhanced (twitch facilitation). Tetanic pulses (50 Hz) to the nerve were followed by post-tetanic twitches of increased amplitude (post-tetanic twitch potentiation, PTP). Hypoxia little affected the twitch facilitation but abolished PTP at both temperatures. These effects differed from those of DNP and ouabain in some ways. Thus, present experiments indicate that hypoxia selectively influences the process which is responsible for the PTP phenomenon rather than for the twitch facilitation. It is possible that the mechanism by which hypoxia would accumulate intracellular Ca2+ may be included in the process through which PTP occurs.

journal of toxicological sciences

Effects of hypoxia, 2,4-dinitrophenol and ouabain on twitch potentiation elicited following conditioning pulses in the mouse phrenic nerve-diaphragm preparation.