ABSTRACT
In acute experiments on anesthetized rats, acetylcholine (Ach) constricts hepatic venous vessels, causing blood mobilization from the liver, and dilates the sphincters of hepatic veins at the exit from this organ, contributing to the intensification of the outflow of blood deposited in the liver. Vasoconstrictor reactions of capacitive vessels of the liver to Ach are realized through M-cholinoreceptors on endotheliocytes with further involvement of messenger, possibly noradrenaline, which activates alpha-adrenoreceptors on smooth muscle cells (SMC) of capasitive vessels. Dilation of Hv sphincters is carried out due to Ach-induced release of messenger in the vessel wall, probably adrenaline, which in turn activates beta-adrenoreceptors on SMC of the Hv. It is possible, that in such reaction partially involved NO.
Subject(s)
Acetylcholine/pharmacology , Hepatic Veins/drug effects , Liver/drug effects , Muscle, Smooth, Vascular/drug effects , Vasoconstriction/drug effects , Adrenergic Antagonists/pharmacology , Animals , Atenolol/pharmacology , Blood Pressure/drug effects , Dioxanes/pharmacology , Endothelial Cells/drug effects , Endothelial Cells/metabolism , Endothelium, Vascular/drug effects , Endothelium, Vascular/metabolism , Hepatic Veins/metabolism , In Vitro Techniques , Liver/blood supply , Muscle Contraction/drug effects , Muscle, Smooth, Vascular/metabolism , Phentolamine/pharmacology , Rats , Receptors, Adrenergic, alpha/metabolism , Receptors, Adrenergic, beta/metabolism , Receptors, Muscarinic/metabolism , Splanchnic Circulation/drug effectsABSTRACT
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.
