https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:12328 2+ concentration ([Ca²⁺]_i), through enhancing extracellular Ca²⁺ entry and Ca²⁺ release from the sarcoplasmic reticulum, processes that are intimately linked with mitochondria. This study examined the effects of oxytocin on mitochondrial function. This was achieved by measuring the ratiometric JC-1 fluorescence signal in isolated myometrial cells, which provides a relative measure of the mitochondrial membrane potential (ψ_m), and also by loading the cells with Oregon Green BAPTA-AM to examine changes in [Ca²⁺]_i. Oxytocin (1 nm) depolarized the ψ_m to 73.8 ± 3.7% of the control value (P < 0.05; perfused for 11 min) and also caused a transient increase in [Ca²⁺]_i. The depolarization of mitochondrial membrane potential was effectively reversed by 2-aminoethoxydiphenyl borate, nifedipine, Ca²⁺-free solution or oligomycin, with the ratiometric JC-1 fluorescence signal becoming no different from the control value in all cases (i.e. P > 0.05). The reduction in ψ_m is likely to occur at least in part through the oxytocin-induced increase in [Ca²⁺]_i, causing enhanced mitochondrial uptake of Ca²⁺ and resultant dissipation of the mitochondrial electrochemical gradient. ATP synthase is also stimulated, which would further contribute to a decrease in ψ_m.]]> Sat 24 Mar 2018 08:11:37 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:11410 Sat 24 Mar 2018 08:11:11 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:11513 Sat 24 Mar 2018 08:11:08 AEDT ]]>