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We used liquid chromatography for analysis of fatty acids (FA) in lipids of erythrocytes of patients with hypertensive disease (HD) with normo- (group 1) and hyperlipidemia (group 2). Abnormalities of FA composition of erythrocyte lipids were revealed in both groups. In group 1 we found deficit of polyenic acids of omega-6 family, accumulation of Mead acid - prostanoid precursor with pronounced vasoconstrictor and pro inflammatory properties. In group 2 we noted more profound rearrangement of lipid matrix of erythrocyte membrane manifested as deficiency of omega-3 polyenic acids, accumulation of palmitinic and arachidonic acids. Preponderance of saturated FA in erythrocytes and deficiency of polyenic acids might evidence for pathology of their ligand-receptor transport into the cell. Blockade of active FA transport initiates formation of HD, promotes accumulation of atherogenic fractions of lipoproteins in blood. These results evidence for important pathogenetic role of FA in development of hypertension.

Effects of several acyclic eicosanoids (which are formed from arachidonic acid under the action of 5- and 12-lipoxygenases) on desensitization of somatic cholinoreceptors of Helix lucorum RPa3 and LPa3 neurons were studied by means of two-electrode voltage clamp technique. The substances under study were: leukotrienes B4, C4, 12(S)-hydroxy-(5Z,8Z,10E,14Z)-eicosatetraenoic acid (12-HETE), threo- and erythro-epimers of hepoxilin B3. Cholinoreceptor plasticity was evaluated by a degree of depression of inward current, induced by rhythmical local ACh applications on the soma with intervals 55-180 sec. Leukotrienes B4 and C4 intensified cholinoreceptor plasticity. Inhibitor of inositol-1,4,5-trisphosphate-dependent (IP3-d) mobilization of deposited Ca2+, TMB-8, prevented the effect of leukotriene C4. 12-HETE, threo- and erythro-epimers of hepoxilin B3 did not change plasticity. A conclusion is made that cholinoreceptor plasticity is controlled by leukotrienes B4 and C4. One of the regulatory pathways includes IP3-d Ca-mobilization. Eicosanoids from 12-lipoxygenase pathway (12-HETE, threo- and erythro-epimers of hepoxilin B3) do not participate in this intracellular regulatory mechanism.

The effects of two acyclic derivatives of arachidonic acid which are formed under the action of 5- and 12-lipoxygenases 5(S)-hydroxy-(6,8Z,11Z,14Z)-eicosatetraenoic acid (5-HETE) and (8R/S)-hydroxy-(11S,12S)-epoxy-5Z,9E,14Z-eicosatrienoi c acid (hepoxilin A3) on extinction of inward current evoked by local acetylcholine (ACh-current) application on soma of Helix lucorum RPa3 and LPa3 neurons were studied by the double-electrode voltage clamp technique. It was shown an increase in ACh-current extinction by 5-HETE. Hepoxilin A3 did not influence cholinoreceptor plasticity. The present results confirm earlier assumptions concerning the regulation of cholinoreceptor plasticity by acyclic eicosanoids which were formed from arachidonic acid under the influence of 5-lipoxygenase and the lack of 12-lipoxygenase metabolites in this regulation.

8Z,11Z,14Z-Eicosatriene-5-ynoic acid and its tritium-labelled analogue, [5,6-3H]arachidonic acid, have been synthesized on the basis of acetylenic compounds. [5,6-3H]Arachidonic acid has been used as substrate for the enzymatic synthesis of [5,6-3H]PGE2 and [5,6-3H]PGF2 alpha.