Child protection or professional self-preservation by the baby nurses? Public health nurses and child protection in Ireland

In Fura-2 loaded-single guinea pig adrenal chromaffin cells, muscarine, nicotine and KCl all caused an early peak rise in intracellular Ca concentration (Ca2+]i) followed by a sustained rise. In Ca(2+)-free solution, muscarine, but neither nicotine nor KCl, caused a transient increase in Ca2+]i, which was partially reduced by preceding application of caffeine or by treatment with ryanodine plus caffeine. In voltage-clamped cells at a holding potential of -60 mV, the muscarine-induced Ca2+]i rise, especially its sustained phase, decreased in magnitude. Intracellular application of inositol 1,4,5-trisphosphate caused a transient increase in Ca2+]i and inhibited the following Ca2+]i response to muscarine without affecting responses to nicotine and a depolarizing pulse. Muscarine evoked membrane depolarization following brief hyperpolarization in most cells tested. There was a significant positive correlation between the amplitude of the depolarization and the magnitude of the sustained rise in Ca2+]i. Muscarine-induced sustained Ca2+]i rise was much greater in the current-clamp mode than that in the voltage-clamp mode. The sustained phase of Ca2+]i rise and Mn2+ influx in response to muscarine were suppressed by a voltage-dependent Ca2+ channel blocker, methoxyverapamil. These results suggest that stimulation of muscarinic receptors causes not only extracellular Ca2+ entry, but also Ca2+ mobilization from inositol 1,4,5-trisphosphate-sensitive intracellular stores. Voltage-dependent Ca(2+)-channels may function as one of the Ca2+ entry pathways activated by muscarinic receptor in guinea pig adrenal chromaffin cells.