Inhibitory effect of hypoxic condition on acetylcholine release is partly due to the effect of adenosine released from the tissue.
Isolated longitudinal muscle strip with Auerbach's plexus attached was used to study the stimulation-evoked release of 3H-acetylcholine (3H-ACh) under normoxic and hypoxic conditions. Hypoxia reduced the release of ACh. Theophylline, a purinoceptor P1 antagonist and vinpocetine, an antiischemic compound partly reversed the effect of hypoxia. Unlike theophylline, the effect of vinpocetine was not mediated via adenosine action, since it failed to affect the presynaptic action of adenosine, and the effect of theophylline and vinpocetine was additive. When they were added together the effect of hypoxia was almost completely antagonized. Dipyridamole, an adenosine uptake inhibitor, potentiated the effect of hypoxia and the presynaptic inhibitory action of adenosine on ACh release. Evidence was obtained that the effect of hypoxia is at least partly due to adenosine formed from purine nucleotides.
Milusheva
E
E
Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest.
Sperlágh
B
B
Kiss
B
B
Szporny
L
L
Pásztor
E
E
Papasova
M
M
Vizi
E S
ES
D000109:Acetylcholine / Q000378:metabolism*; D000241:Adenosine / Q000378:metabolism* / Q000494:pharmacology; D000818:Animals; D004176:Dipyridamole / Q000494:pharmacology; D005260:Female; D006168:Guinea Pigs; D000860:Hypoxia / Q000378:metabolism*; D066298:In Vitro Techniques; D008297:Male; D009132:Muscles / Q000187:drug effects / Q000378:metabolism*; D014748:Vinca Alkaloids / Q000494:pharmacology
D014748:Vinca Alkaloids; C013983:vinpocetine; D004176:Dipyridamole; D000241:Adenosine; D000109:Acetylcholine