RESUMEN
Transfer factor (TF) of immune reactivity (10(-5) - 10(-3) mg/ml) to diphtheria-tetanus anatoxin modulates slow waves and spontaneous contractile activity of non-atropinized smooth muscle stripes (SMS) of guinea-pig taenia coli. TF (10(-4) mg/ml) transforms slow waves into stable depolarization and tonic contraction. After SMS atropinization, the substance acts in the same way. In the presence of methylene blue (10(-5) M), a guanylatecyclase blocker, FT induces transitory increase of SMS muscle tone, which is followed by their stable relaxation. ATP and UTP, purinoceptors agonists, evoke substantial hyperpolarization of smooth muscle cells membrane and their relaxation. FT enhances post-inhibitory excitation in SMS. In the presence of acetylcholine (10(-5) M) FT (10(-4) mg/ml) transforms the inhibitory ATP action on tonic contraction into excitative. This substance (10(-5), 10(-4) mg/ml) enhances Ca2+ mobilization from ryanodine-sensitive calcium store, inhibits the release of these cations from IP3-sensitive calcium store of sarcoplasmic reticulum. TF demolishes the inhibitory actions of sodium nitroprusside (nitric oxide donor), and noradrenaline in taenia coli smooth muscles.
Asunto(s)
Colon , Toxoide Diftérico/inmunología , Relajación Muscular/efectos de los fármacos , Músculo Liso , Neurotransmisores/farmacología , Toxoide Tetánico/inmunología , Factor de Transferencia/farmacología , Animales , Calcio/metabolismo , Colon/efectos de los fármacos , Colon/inmunología , Colon/inervación , Estimulación Eléctrica , Cobayas , Técnicas In Vitro , Potenciales de la Membrana/efectos de los fármacos , Músculo Liso/efectos de los fármacos , Músculo Liso/inmunología , Músculo Liso/inervación , Retículo Sarcoplasmático/efectos de los fármacos , Retículo Sarcoplasmático/inmunología , Factor de Transferencia/inmunologíaRESUMEN
Immune-active substance of Staphylococcus aureus, cell-bound protein A (CBPA), enhances the acetylcholine- or hyperpotassium (K+) Krebs solution-evoked excitation in Taenia coli smooth muscles. CBPA increases caffeine- and carbachole-evoked Ca2+ signals in smooth muscle cells suspension, loaded with indo-1, and also caffeine- and acetylcholine-evoked contraction in smooth muscles slices. Against a background of CBPA-suppressed action of sodium nitroprusside, ATP evokes the membrane depolarization. CBPA in small concentrations potentiates ATPase (Mg2+,Ca2+-; Mg2+- and Mg2+- in the presence of EGTA) activity of actomyosin in the smooth muscles.
Asunto(s)
Señalización del Calcio/efectos de los fármacos , Músculo Liso/efectos de los fármacos , Miosinas/metabolismo , Proteína Estafilocócica A/farmacología , Staphylococcus aureus/metabolismo , Acetilcolina/farmacología , Potenciales de Acción/efectos de los fármacos , Animales , Cafeína/farmacología , Carbacol/farmacología , Células Cultivadas , Colon/citología , Colon/efectos de los fármacos , Colon/enzimología , Colon/metabolismo , Cobayas , Contracción Muscular/efectos de los fármacos , Músculo Liso/citología , Músculo Liso/enzimología , Músculo Liso/metabolismo , Nitroprusiato/farmacologíaRESUMEN
Cell-bound protein A (CBPA), an immune-active substance of Staphylococcus aureus was ascertained to depolarize membrane of taenia coli smooth muscle (SM) cells, depress ATP inhibiting action (or uridinetriphosphate (UTP)) and sodium nitroprusside (SNP). ATP or UTP-induced membrane hyperpolarization increased during first minutes of CBPA exposure. Bacterial substance enhanced and then inhibited fast component of nicotine-induced relaxation of histamine-activated smooth muscles. This enhancement was inhibited by N(omega)-nitro-Larginine, a NO-syntase blocker. CBPA decreased ATP inhibiting action upon histamine-induced contraction, but enhanced cholinergic SM excitation. All these processes are reversible.
Asunto(s)
Adenosina Trifosfato/farmacología , Contracción Muscular/efectos de los fármacos , Músculo Liso/efectos de los fármacos , Óxido Nítrico/fisiología , Proteína Estafilocócica A/farmacología , Staphylococcus aureus/metabolismo , Animales , Membrana Celular/efectos de los fármacos , Membrana Celular/fisiología , Colon/efectos de los fármacos , Colon/inervación , Inhibidores Enzimáticos/farmacología , Cobayas , Técnicas In Vitro , Potenciales de la Membrana/efectos de los fármacos , Potenciales de la Membrana/fisiología , Contracción Muscular/fisiología , Músculo Liso/inervación , Donantes de Óxido Nítrico/farmacología , Óxido Nítrico Sintasa/antagonistas & inhibidores , Nitroprusiato/farmacología , Uridina Trifosfato/farmacologíaRESUMEN
The G-protein-dependent intracellular signal cascades of excitation in longitudinal and circular intestinal smooth muscles (SM) are compared and summarized in the present review. The key mechanism of excitation in longitudinal SM is an activation of electro-mechanical coupling, in that G-proteins, phospholipase A2, arachidonic acid, membrane-bound cyclic adenosine diphosphoribose and Ca2+ are involved. We observed the role of arachidonic acid-activated chorine and voltage-dependent Ca2+ -channels (L-type) in Ca2+ mobilization in these muscle cells. In contrast to longitudinal, the main mechanism of agonist-induced excitation in circular SM is connected with activation of key methabotropical processes. The role of Rho-kinase in mechanisms of Ca2+ --sensitization of contractile apparatus in SM is also shown in this review. A comparative analysis of involvement of different links of signal cascades in initial and sustained phases of contraction in longitudinal and circular SM are also reviewed.
Asunto(s)
Mucosa Intestinal , Intestinos , Músculo Liso , Receptores de Neurotransmisores/metabolismo , Animales , Proteínas de Unión al GTP/metabolismo , Humanos , Mucosa Intestinal/metabolismo , Intestinos/citología , Intestinos/enzimología , Péptidos y Proteínas de Señalización Intracelular/metabolismo , Canales Iónicos/metabolismo , Contracción Muscular , Músculo Liso/citología , Músculo Liso/enzimología , Músculo Liso/metabolismo , Proteínas Serina-Treonina Quinasas/metabolismo , Transducción de Señal , Quinasas Asociadas a rhoRESUMEN
The mechanisms of bacterial substances (protein A, peptidoglican Staphylococcus aureus), bacterium toxins (St. aureus, Corynebacterium diphtheriae, Shigella dysenteriae, Clostridium botulinum, Clostridium tetani, Vibrio choleral), transfer factor of immune reactivity to Staphylococcus aureus upon the key link (acetylcholine-, ATP-, inositol-1,4,5-triphosphate-, ryanodin-sensitive receptors, G-proteins, Ca2+, K(+)-transporting systems, second messengers) in the chain of signal conduction of excitatory and inhibitory agonists in excitable cells were examined. The action of these immune-active substances upon contractile proteins ATP-ase activity and protein synthesis was also discussed.