Abstract
Hypoxia is suggested to increase intracellular Ca<2+>, there-by affecting cellular functions. If this is the case, the effect would be modified by other treatments which also elevate intracellular levels of Ca<2+>. 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 Ca<2+>. 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°C but not at 24°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 Ca<2+> may be included in the process through which PTP occurs.
