[Prostaglandin E2 as a lipophilic allosteric modulator of the Na pump]. / Prostaglandin E2 kak lipofil'nyi allostericheskii moduliator Na-nasosa.

Curves of inhibition of rat brain Na, K-ATPase and K-pNPPase by prostaglandin E2 (PGE2) showed a sigmoidal shape with nH for PGE2 of 1.4 +/- 0.1 and 1.3 +/- 0.1, respectively. The desensitization of the enzymes with 0.25 M urea (4 degrees, 15 min) caused a loss of their cooperative interaction with PGE2. 2.0 mM PGE2 shifts the temperature break in the Arrhenius plots for the ATPase from 19.8 degrees to 23 degrees and simultaneously increased the Ea below the break by 9.5 kcal/mol. After treatment of the ATPase with phospholipase A2 PGE2 showed no cooperative interaction with the enzyme. Modulation of membrane enzymes by means of the surrounding lipid phasic state appears to be the general mechanism of their indirect allosteric regulation.

[Effect of psychotropic drugs on cerebral Ca-activated ATPase in vitro]. / Vliianie psikhotropnykh sredstv na Ca-aktiviruemye ATF-azy mozga in vitro.

Neuroleptics, particularly haloperidol and perphenazine, inhibit the activity of brain Ca, Mg-ATPase to a greater extent than the antidepressants benactizin and amphetamine. The actomyosin-like Ca-ATPase is far less sensitive to the psychotropic drugs than Ca,Mg-AtPase. It is suggested that the inhibition of brain Ca,Mg-AtPase by neuroleptics may play a certain role in their antipsychotic action.

[Comparative effect of psychotropic agents on orienting-motor responses and cerebral Na,K-ATPase activity in vivo]. / Sravnitel'noe deistvie psikhotropnykh sredstv na orientirovochno-dvigatel'nye reaktsii i aktivnost' Na, K-ATF-azy mozga in vivo.

Levomepromazine, chlorpromazine (10 and 30 mg/kg), etaperaxine, haloperidol (3 and 10 mg/kg) inhibited the exploratory-motor reactions of rats and the brain Na, K-ATPase activity an hour after their administration. The effects of tranquilizers as well as of antidepressants on the exploratory reactions and on the enzyme activity were not found to stand in a clearcut relation to each other. The stimulating effect of amphethamine (3 mg/kg) was accompanied by activation and suppressive action (10 mg/kg)--by inhibition of the enzyme. It is suggested that the inhibition of the brain Na, K-ATPase activity by psychotropic drugs may play a role in the mechanism of their sedative action.

[Comparative study of the effect of some psychotropic substancces on the activity of brain Na+, K+-ATPase in vitro]. / Sravnitel'noe izuchenie vliianiia nekotorykh psikhotropnykh veshchestv na aktivnost' Na+, K+-ATF-azy mozga in vitro

The activity of Na+, K+-ATPase from bovine brain in vitro was studied as affected by some neuroleptics (levomepromazine, chlorpromazine, perphenazine and haloperidol), antidepressants (imipramine and iproniazid) and psychostimulants (amphetamine) as well as by benactyzine and procaine. The degree of the enzyme inhibition by these drugs estimated by means of I 50 and apparent inhibitor constants (Ki) or rate constants (k) was different. Sensitivity of the brain Na+, K+-ATPase to the drugs decreased in the following order: levomepromazine, chlorpromazine, perphenazine, haloperidol, imipramine, iproniazid, benactyzine, procaine and amphetamine. Competition for the enzyme was revealed between sodium and some of the drugs investigated (levomepromazine, chlorpromazine, perphenazine and impramine) as well as between potassium and other drugs (haloperidol, genactyzine and amphetamine). It is suggested that the inhibition of the brain Na+, K+-ATPase by psychotropic drugs may be a part in the biochemical mechanism of their sedative-tranquilizing activity.