Aims: 

To investigate the influence of Ach on hepatic blood circulation and to find out mechanisms of its action on venous vessels of the rat liver.

Methods: 

In acute experiments on anesthetized rats (by uretan – 1g/kg) the blood pressure in carotid artery (AP) and in portal vein (PV), local blood flow (LBF) in liver and changes in liver's blood volume (LBV) were registrated on intraportal administration of Ach. The thensometry was used for registration of constriactile activity of isolated and perfused by warmed Tyrode solution rat portal vein.

Results: 

Ach (1 mkg/kg) caused decrease in AP on 35%, LBV on 24% and LBF on 22% (p < 0.05), and increase in Ppv on 38, that testifies to constricting intrahepatic venous vessels, hepatic veins and, probably, sinusoids. Reactions AP and LBV were removed to initial level by M-chlinolitic atropin (1mg/kg), and changes Ppv were blocked on 60-78% by a-adrenoreceptors antagonist phentholamine (2 mg/kg). Atropin (1·10^-8 mol/l) completely blocked Ach-induced constriction of isolated PV, nicotinic blocker tubocurarin (1.5·10⁴ mol/l) – on 50%, and phentolamine (1·10^-4 mol/l) – on 40% (p < 0.05). At the same time Ach (1·10^-5 mol/l) caused relaxation of hepatic vein (HV) on 1.4 ± 0.5 [mcy]H (p < 0.05), wich were atropin- and tubocurarin-resistant, but sensitive to b₁-adrenolytics athenolol.

Conclusion: 

Constrictor action Ach on PV can be realized through M-, N-cholinoreceptors and a-adrenoreceptors vessel wall. Adrenergic way, but without involving cholinoreceptors are realised vasoconstrictor influence of Ach, probably, on pre- and postsinusoidal small veins too, and vasodilatator effect of Ach on HV.