Fig. 3

Betaine induces calcium influx from the extracellular milieu. a 10 mM Betaine in nominally free [Ca²⁺]_o, followed by 10 µM Thapsigargin. b 10 mM Betaine in 2 mM [Ca²⁺]_o. c 400 nM Bay-K 8644, wash and restoration of the initial condition (time break axis), followed by 10 mM Betaine in 2 mM [Ca²⁺]_o. d 10 mM Betaine followed by 400 nM Bay-K 8644 in 2 mM [Ca²⁺]_o. e 10 min incubation (time break axis) with 30 µM Nimodipine, followed by 10 mM BET administration (2 mM [Ca²⁺]_o). f 30 µM Nifedipine incubation for 10 min (time break axis) and subsequent treatment with 10 mM BET (2 mM [Ca²⁺]_o). g Administration of 250 µM LaCl₃ and 5 min incubation (time break axis), followed by 10 mM BET (2 mM [Ca²⁺]_o). h Fluorescence intensity changes of Fura-2/AM recorded at the calcium insensitive excitation wavelength of 360 nm (λ_em = 510 nm), after the administration of 2 mM MnCl₂ in presence of 10 mM BET (2 mM [Ca²⁺]_o). These results lead to the hypothesis that BET induced calcium influx through L-type voltage-dependent Ca²⁺ channels. All the stimuli were added at the time points indicated by the arrows in the graphs. Each graph shows the intracellular calcium changes of a cells representative group from at least 3–6 independent experiments. Each line in the graphs display a single cell behavior. The table reported in the graph summarizes the number of analyzed cells together with the percentage of responsiveness and the mean [Ca²⁺]_i increases for all the experiments here described