[The blood plasma kinin system in rabbits at the early stages of postnatal ontogenesis].
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Biomedical subjects
Publications and source records attributed to V I Kiselev.
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The recombinant plasmid pKP145 PL has been constructed containing the gene for aminoglycosidephosphotransferase (APT). Expression of the APT gene is under the control of lambda bacteriophage PL promoter. Escherichia coli cells harbouring this plasmid synthesize APT in quantity up to 13-15% of the total cellular protein. The technique for isolation of APT from superproducing cells has been elaborated. Preparations of the enzyme devoid of contaminating bacterial proteins have been obtained.
Experimental and clinical studies have shown that surgical procedures on the liver and biliary tracts particularly accompanied by compression of the hepatoduodenal ligament in order to perform temporal hemostasis are followed by activation of kinin-formation. In most traumatic operations it exceeds the limits of regulatory mechanisms and is a cause of hemodynamic disturbances. Protease inhibitors are recommended to prevent such complications.
A method for the evaluation of the aminoglycoside phosphotransferase activity in bacterial colonies directly is described. The method is based on the ability of the enzyme to modify the substrate immobilized on carboxymethylcellulose paper. The sensitivity and accuracy of the method were tested by comparing the results of the present assay to those obtained with conventional procedures. The method seems to be particularly useful for the detection within a bacterial population producing aminoglycoside phosphotransferase of those cells which do not make the enzyme and for rapid determination of the relative levels of enzyme produced by different clones.
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The effects of thymus ablation and injection of thymalin on the blood plasma kallikrein-kinin system were studied. Thymus ablation was followed by activation of kinin formation, evidenced by an elevation of the total kallikrein activity and drop of the kininogen level. Injection of thymalin into thymectomized animals makes the characteristics under study return to normal.
Sympathetic activation results in activation of kallikrein-kinin system and in suppression of the sensitivity of the cardiovascular system to bradykinin in animals. Prevalence of cholinergic effects over adrenergic ones suppresses formation of kinin and increases its inactivation. Sympathectomy enhances the sensitivity of cardiovascular system to bradykinin.
The spontaneous recovery of activity of tet gene deleted of the promoter region was studied. Plasmid pBRS188 was used as a model for studying this problem. The plasmid has the fragment of tet gene of pBR322, from which it originates, between the sites of restriction endonucleases EcoRI and HindIII cleavage resulting in inactivation of tet promoter. E. coli cells harbouring the plasmid were shown to revert the TcR phenotype with the frequency 10(-9). The gene activation coincided with intraplasmid recombination revealed by restriction analysis. In some cases the recovery of tet gene activity coincided with the formation of multimeric plasmids.
The effects of kallikrein, thrombin, and plasmin on interaction of acetylcholine and noradrenaline with receptors of the isolated portal vein of guinea-pigs were studied. The functional activity of receptors was studied by the pharmacokinetic method. It was found that kallikrein and thrombin do not disturb the kinetics of agonist interaction with receptors, whereas the magnitude of isometric vascular contractions dramatically decreased after plasmin treatment and becomes disproportionate to the concentration of neurotransmitters. Exposure of the portal vein to kallikrein or thrombin caused different changes in the sensitivity and quantity of active cholino- and adrenoreceptors. These proteolytic enzymes reduced the sensitivity of receptors to noradrenaline and increased it to acetylcholine. Exposure to kallikrein brought about a decrease in the quantity of active cholinoreceptors and a rise in the number of adrenoreceptors. The treatment of the vessels with thrombin resulted in a decrease in the number of active adrenoreceptors. The number of active cholinoreceptors remained unchanged.
The reactions of cardiovascular system at various intensities of kininogenesis were studied with the aid od dose--effect curves of bradykinin hypotensive action. Correlations were found between the intensity of kinin--induced reaction and the level of some components of the blood Kallikrein-kinin system. Activation of kininogenesis was accompanied by a decrease of kinin-reactivity whereas inhibiton of kinin formation was followed by an augmentation of the hypotensive kinin-induced reaction.
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A study was made of bradykinin action on isolated vessels of the dog and guinea-pig. Regularities of bradykinin interaction with smooth muscle structures were evaluated with the aid of the curves showing the dependence of the effect on the concentration. The action of bradykinin was demonstrated to be receptor in character. Regularities of bradykinin interaction with the receptors are determined by the region and type of the vessels.
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The equation describing kinetics of interaction between bradykinin and cardiovascular receptors resembles the equations describing depressive adrenergic and some cholinergic reactions in dogs, rabbits and white rats. In this study of bradykinin receptor state, in order to describe quantitatively hypotensive action of different bradykinin doses on interaction of this peptide with receptors, bradykinin had to be injected intraaortally. The data obtained revealed that the greatest efficiency of kininergic reaction occurred in dogs whereas the least--in white rats.
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