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The mechanisms of the negative consequences of general anaesthetics action on the nervous system have been studied in detail, but regarding smooth muscle function, such issues have not yet been sufficiently addressed. In this study, we investigated the effect of the general intravenous anaesthetic ketamine on the level of intracellular calcium in isolated ileum myocytes and the contractile activity of smooth muscle strips of the mouse small intestine. The concentration of intracellular calcium in cells was measured using the Ca2+-sensitive fluorescent dye Fura-2, and tensiometry was used to record the contractile activity of smooth muscles. It was shown that ketamine at a concentration of 100 μM significantly, by 40%, suppressed carbachol-induced contractile reactions of the ileum. The inhibitory effect correlated with the suppression of the intracellular calcium responses to carbachol in isolated smooth muscle cells after the addition of ketamine to the extracellular solution, which was by 65% on average. These results contribute to our better understanding of the possible membrane and intracellular mechanisms of the development of post-surgical intestinal motility disorders. [ABSTRACT FROM AUTHOR]

The work is devoted to the study of the effect of Staphylococcus aureus peptidoglycan on the main parameters of myometrial contractions and the mechanism of this influence. The research was carried out by tensometry and calcimetry methods. The results of the experiments demonstrated that peptidoglycan modulates all the main parameters of contractions of the non-pregnant rat uterus, including increasing their amplitude and duration by 10 and 30%, respectively, mainly by prolonging the relaxation phase (56.7 ± 1.6%): myometrial band relative to quickly shrunk and relaxed for a long time. Application of peptidoglycan on freshly isolated uterine myocytes for 5 min led to a periodic increase in their intracellular content of calcium ions. Peptidoglycan enhanced myometrial contractions caused by hyperpotassium solution at a concentration of 60 mmol. Administration of 1 μmol of nifedipine, a blocker of potential-directed L-type calcium channels, suppressed spontaneous contractions enhanced by peptidoglycan. These changes in myometrium contractility of on the background of peptidoglycan action occur not only due to increased transmembrane calcium intake, but also its mobilization from the sarcoplasmic reticulum. [ABSTRACT FROM AUTHOR]

Calcium is an important signaling element and universal intracellular messenger and the determining ion in the process of Excitation-Contraction Coupling. This review describes calcium receptors at this process in cardiomyocytes. The main sources of increase of intracellular calcium level is entry from extracellular medium by dihydropyridine receptors and release from internal stores, in particular, from the sarcoplasmic reticulum (SR) via activation of ryanodine receptors. The absence of a transverse tubular network in the atria myocytes makes the Ca2+ release process specific to the ventricular cells of the myocardium. Atrial myocytes, but not ventricular, also express inositol triphosphate receptors that complement the regulation of Ca2+ signal. The calcium receptors described in this review reveals in more detail of Excitation-Contraction Coupling and details Ca2+ - dependent regulation of cardiomyocyte. [ABSTRACT FROM AUTHOR]