Effect of (2-benzoylethyl)trimethylammonium and vesamicol on acetylcholine and prostaglandin release from human placental explants.
Human placental explants were incubated in the presence of physostigmine (3.08 microM), and release of acetylcholine (ACh) and prostaglandin (PG) were measured in the fourth hour by bioassay and radioimmunoassay, respectively. The choline acetyltransferase inhibitor (2-benzoylethyl)trimethylammonium (100 microM, n = 6) significantly reduced ACh release by 36 +/- 6%, PGE2 release by 23 +/- 8% and PGF2 alpha release by 29 +/- 10%. The inhibitor of vesicular acetylcholine storage, vesamicol (100 microM, n = 7), significantly reduced ACh release by 22 +/- 4%, PGE2 release by 46 +/- 13% and PGF2 alpha release by 32 +/- 9%. In the absence of physostigmine, ACh release was reduced by 89 +/- 2%, whereas PG release did not change compared with that in the presence of physostigmine. The presence of atropine (14.4 microM) did not affect PG release. These results suggest that if there is a relationship between human placental production of ACh and PGs, it does not appear to depend on muscarinic receptor activation or the activity of placental cholinesterase.
Chen
Y S
YS
Monash Perinatal Unit, Department of Obstetrics and Gynaecology, Monash University, Clayton, Vic., Australia.
Brennecke
S P
SP
Rook
T J
TJ
King
R G
RG
D000109:Acetylcholine / Q000031:analogs & derivatives* / Q000037:antagonists & inhibitors* / Q000378:metabolism / Q000494:pharmacology; D015237:Dinoprost / Q000037:antagonists & inhibitors* / Q000378:metabolism; D015232:Dinoprostone / Q000037:antagonists & inhibitors* / Q000378:metabolism; D005260:Female; D006801:Humans; D009924:Organ Culture Techniques; D010830:Physostigmine; D010880:Piperidines / Q000494:pharmacology*; D010920:Placenta / Q000187:drug effects* / Q000378:metabolism; D011247:Pregnancy
D010880:Piperidines; C017058:(2-benzoylethyl)trimethylammonium; C006189:vesamicol; D010830:Physostigmine; D015237:Dinoprost; D015232:Dinoprostone; D000109:Acetylcholine