The present study investigated the acute effects of taurine on intracellular Ca2+ ([Ca2+]i) in normal and diabetic cardiac myocytes. [Ca2+]i was monitored using fura-2 in single myocytes isolated from control or streptozotocin-treated rats and paced at frequencies between 0.33 Hz and 2.0 Hz in the absence or presence of 20 mM taurine. Increasing stimulus frequency resulted in significant increases in resting and peak [Ca2+]i, and amplitude of the Ca2+ transient in both control and diabetic myocytes. The amplitude of the Ca2+ transient and the extent of its increase with increasing frequency was, however, significantly lower in the diabetic myocytes. Taurine significantly increased resting [Ca2+]i, peak [Ca2+]i, and the amplitude of the Ca2+ transient in both control and diabetic myocytes at all stimulus frequencies examined. The degree of potentiation of the Ca2+ transient decreased with increasing stimulus frequency in control cells but not in diabetic cells. In the absence of taurine the decay of the Ca2+ transient was significantly slower in diabetic than control myocytes. Taurine was without significant effect on the time course of the Ca2+ transient decay in control cells, however, in diabetic cells it significantly accelerated the rate of decay. The data demonstrate directly that taurine is able to increase [Ca2+]i and the amplitude of the Ca2+ transient in both normal and diabetic cardiac myocytes. In addition several of the effects of taurine appeared to be more pronounced in diabetic than control cells.
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