[ROLE OF THROMBOXANE AND LEUKOTRIENES IN MECHANISMS OF CONTRACTILE REACTIONS OF PORTAL VEIN, INDUCED BY ACETYLCHLINE AND PHENYLEPHRINE].

Effects of picotamide and zileuton on tonic contractile activity of the rat portal vein preparations, induced by acetylcholine (2.10(-5) mol/1) and phenylephrine (5.10(-7) mol/1) were investigated. Conversion of arachidonic acid products (prostaglandins, leukotrienes) synthesized by endothelial cells, plays an important role in the local regulation of vascular tone. The compounds formed in a cascade of enzymatic transformations can modulate the effect of other vasoactive factors. Picotamide (6,5.10(-5) mol/1) - thromboxane receptor and thromboxane -synthase blocker - depress acetylcholine-induction tonic contraction of isolated segments of portal vein with intact endothelium by 29% and norepinephrine-induction reduction of 45% relative to the control values. The obtained results indicate a participation of thromboxane and/or endoperoxide H2 in this reaction. Partial inhibition of the contractions by 5-lipoxygenase blocker zileuton(4,2.10(-5) mol/1) at 23% relative to control values suggests, that products of lipoxigenase pathways of arachidonic acid conversion are involved in mechanisms of specified reactions. These data indicate complex mechanisms of regulation of vascular tone of the portal vein, which play an important role eicosanoids. Further study of these mechanisms is necessary for the formation of basic knowledge, as well as to elucidate the mechanisms of occurrence and development of pathological conditions of vessels and the development of methods of their correction.

[Participation of eicosanoids in the mechanisms of contractile reactions of the portal vein to adrenaline and noradrenaline].

The influence of indometacine (7 x 10(-8)M) on the tonic contractile activity of the isolated rat portal vein (PV) under the action of adrenaline (1 x 10(-5)M) and noradrenaline (5 x 10(-6)M) was studied. Indometacine decreased the amplitude of noradrenaline-induced tonic constriction of PV with intact endothelium and produced no effect on constriction of vessels with denuded endothelial layer. The results suggest that these reactions are mediated by endothelial prostanoids. Inhibition of adrenaline-induced constriction of PV preparations with intact and denuded endothelium suggests that the contractile reactions are mediated by prostanoides derived from both endothelial and smooth muscle cells.

[Mechanisms of contractile action of acetylcholine on hepatic veins].

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.

Vasoconstrictor effect of acetylcholine in veins of the liver.

Intraportal acetylcholine administered to narcotized rats produced atropine-resistant constriction of hepatic veins, which was considerably prevented by phentolamine. Sodium nitroprusside produced a vasodilator effect. Similar results were obtained on isolated venous strip from the portal vein: acetylcholine-induced contraction was reduced by 25-50% in the presence of nicotinic receptor antagonist tubocurarine and cholinergic agonist nicotine and by 10% in the presence of tetrodotoxin. Probably, acetylcholine stimulates synthesis and release of a vasoconstrictor transmitter via nicotinic receptors of endothelial cells and/or portal vascular wall nerve terminals.

[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.

[Modulation of electrical and contractile responses of the isolated abdominal aorta in hyperholesterinemia and after treatment with calcium antagonists].

Membrane potential of aorta's endothelium, contractile responses of isolated preparation of the abdominal aorta and their modulation with calcium antagonists were studied at hypercholesterinemia (HHS). Membrane potential has been observed to be slightly depolarized at HHS, and acetylcholine-induced electric and contractile responses were shown to be depressed. Calcium antagonists had positive effect on MP, electric and contractile responses of the preparations of the abdominal aorta of rats with HHS. The most pronounced protective effect of membrane potential and contractile responses at HHS was observed in rats after asparcam using.

[The effect of SR 142801, a blocker of tachykinin NK-3 receptors, on synaptic transmission in the rat caudal mesenteric ganglion]. / Vplyv blokatora SR 142801 takhikininovykh NK3, retseptoriv na synaptychnu peredachu u kaudal'nomu bryzhovomu hanhliï shchura.

Effects of tachykinin NK-3 receptors antagonist SR 142801 on the synaptic transmission in the rat's caudal mesenteric ganglion were investigated using extracellular recording of compound action potentials (CAPs) from the ganglion nerves. It is shown that antagonist of NK-3 receptors SR 142801 (2.5.10(-7) mol/l) decreased the amplitude and square of CAPs obtained by stimulating of intermesenteric nerve (IMN) and leading off from the colonic nerve, after high-frequency stimulation of IMN. It is suggests that tachykinin NK-3 receptors take part in SP-ergic synaptic transmission through the rat's caudal mesenteric ganglion.

[The effects of substance P and capsaicin on synaptic transmission in the peripheral reflex pathways of the rat caudal mesenteric ganglion]. / Efekty substantsiï P ta kapsaitsynu na synaptychnu peredachu u peryferychnykh reflektornykh shliakhakh kaudal'noho bryzhovoho hanhliiu shchura.

Peripheral nerve pathways in the caudal mesenteric ganglion of the rat were found. They preserve synaptic transmission after degeneration of preganglionic nerve fibres. To find the effects of substance P (SP) and capsaicin, the SP antagonist, on the synaptic transmission in peripheral reflex pathways of the caudal mesenteric ganglion rats were investigated using extracellular recording of action potentials from the ganglion nerves. Perfusion of the ganglion by solution containing SP (5 x 10(-7) and 1 x 10(-8) mol/l), facilitated the transmission, while capsaicin (5 x 10(-5) mol/l) inhibited it. The inhibitory effect grew at high-frequency stimulation of peripheral nerves.