[Elucidation of the mechanisms of acetylcholine constrictor action on the portal vein and its intrahepatic branches].
Intraportal administration of acetylcholine (Ach) to anesthetized rats evokes endothelium depended, atropine resistant and phentholamine sensitive constriction of hepatic portal vessels. On the contrary to Ach action sodium nitroprussideresulted in vasodilatation in this vessel. On the isolated segment of portal vein (PV) similar results were obtained; at the same time the blockade of nicotinic acetylcholinic receptors by nicotine (in high concentration), tubocurarine or tetrodotoxine diminished constrictor reactions of PV to Ach. We concluded that described vasomotor effects of Ach in the hepatic portal bed are carried out through nicotinic Ach-receptors localized on endothelial cells and (or) adrenergic neurones in the wall of portal vessels. These cells synthesize and release mediators, possibly, noradrenaline which causes constriction of portal vessels.
Ianchuk
P I
PI
Pasichnichenko
O M
OM
Komarenko
V I
VI
Prykhod'ko
T P
TP
Tsybenko
V O
VO
D000109:Acetylcholine / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D018678:Cholinergic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D004285:Dogs; D066298:In Vitro Techniques; D008099:Liver / Q000098:blood supply*; D009599:Nitroprusside / Q000494:pharmacology; D010477:Perfusion; D011169:Portal Vein / Q000187:drug effects*; D051381:Rats; D014661:Vasoconstriction / Q000187:drug effects*; D014664:Vasodilation / Q000187:drug effects
D018678:Cholinergic Agents; D009599:Nitroprusside; D000109:Acetylcholine