title: [Intracellular signal systems in the epithelium- and endothelium-dependent relaxation of smooth muscles].
abstract: The research of mechanisms of a regulation electrical and contractile of properties of unstriated muscles of an internals remains by an actual problem of modern physiology and medicine. Already now it is possible to state that the efficacy of means of correction of distresses of an internals depends on a degree of a level of scrutiny of these mechanisms. Among physiologically active substances effecting on smooth muscle cells (SM), the special relaxing factor synthesized by endotheliocytes, epithelial cells and SM. Identified by the majority of the explorers as oxide of nitrogen (NO), relaxing factor responds for exhibiting of many myogenic responses of pots and pneumatic routes. The mechanisms of synthesis and implementation of effects of this factor in SM cells up to the extremity are not clarified. The considerable advance in learning mechanisms of operation relaxing factor on SM is connected to discovering of ability of some nitro compounds to replicate NO-dependent relaxing effects in these cells. The main systems of intracellular regulation are involved in mechanisms of implementation endothelial and epithelial local regulatory effects on SM. The majority of the explorers bind an epithelium-dependent release phenomenon SM to an activation of a solvable fraction guanilatcyclase, found in the majority of cells, and effects of cGMP-dependent protein kinases. There are reports on ability of inhibitors NO-sintase to depress a release phenomenon SM of pots and bronchuses, about dependence of a mechanical strain SM of pots and respiratory tract from a contents cGMP in cells. However there are datas giving establishments to guess, that alongside with guanilatciclase in a release phenomenon SM, induced relaxing factors or nitro compounds, the immediate involvement is accepted by cAMP-dependent protein kinases. The most probable point of interaction cAMP and cGMP-dependent processes is phospodiesterase of cyclic nucleotides. It citosolium the enzyme labilized by calmodulin, is capable to carry out a hydrolysis of both cyclic nucleotides, and the affinity native phospodiesterase to cGMP exceeds affinity to cAMP more, than on the order. It is impossible to eliminate immediate interference of NO-dependent processes in a regulation of activity contractile proteins. The ability cGMP-dependent processes to depressing mechanisms of phosphorylation and intensifying of a dephosphorylization of contraktion proteins SM is shown. At these processes can variate and affinity of the acto-miosin complex to ions of calcium, producing a release phenomenon of smooth muscles. On all visibility, production relaxing of the factor and the implementation is epithelial and endothelium-SM of mutual relation in a respiratory tract and pots comes true by modulating influence at the calcium signal system of other systems. For example, production relaxing of the factor by an epithelium and endothelium, being calcium-dependent process, is regulated at involvement calmodulin-similar Ca(2+)-connecting proteins and protein kinase C. Control of tone SM through change of membrane potential relaxing factor carries out by paravariation of potassium conduction of a membrane SM, and, is more probable than all through calcium-dependent and ATP-sensitive components. Potencial-dependent control of a muscle tone comes true through change of efficacy of an operation from a branch of the calcium signal system and calcium pompes at submaximal concentrations of free calcium in citosolium.
authors.affiliation: Siberian Medical University, Tomsk.
authors.forename: L V
authors.initials: LV
authors.lastname: Kapilevich
authors.forename: I V
authors.initials: IV
authors.lastname: Kovalev
authors.forename: M B
authors.initials: MB
authors.lastname: Baskakov
authors.forename: M A
authors.initials: MA
authors.lastname: Medvedev
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D002147:Calmodulin / Q000378:metabolism; D002462:Cell Membrane / Q000502:physiology; D000242:Cyclic AMP / Q000378:metabolism; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism; D006152:Cyclic GMP / Q000378:metabolism; D004553:Electric Conductivity; D004727:Endothelium / Q000378:metabolism / Q000502:physiology; D004848:Epithelium / Q000378:metabolism / Q000502:physiology; D006162:Guanylate Cyclase / Q000378:metabolism; D009126:Muscle Relaxation; D009130:Muscle, Smooth / Q000378:metabolism / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D011493:Protein Kinase C / Q000378:metabolism
chemical_list: D002147:Calmodulin; D009569:Nitric Oxide; D000242:Cyclic AMP; D017868:Cyclic AMP-Dependent Protein Kinases; D011493:Protein Kinase C; D006162:Guanylate Cyclase; D006152:Cyclic GMP; D011188:Potassium; D002118:Calcium