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
In acute experiments on anesthetized rats was shown, that endothelin-1 constricts arterial and portal vessels of the liver, reduces blood flow in the liver, supresses tissue respiration and heat production in this organ. Thus, the level of oxygen pressure in the liver might grow. The influence endothelin-1 on tissue respiration and heat production is mediated through ET(A)-receptors.
