The present study investigated the acute effects of taurine on intracellula
r Ca2+ ([Ca2+](i)) in normal and diabetic cardiac myocytes. [Ca2+](i) was m
onitored using fura-2 in single myocytes isolated from control or streptozo
tocin-treated rats and paced at frequencies between 0.33 Hz and 2.0 Hz in t
he absence or presence of 20 mM taurine. Increasing stimulus frequency resu
lted 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 freque
ncy was, however, significantly lower in the diabetic myocytes. Taurine sig
nificantly increased resting [Ca2+](i), peak [Ca2+](i), and the amplitude o
f the Ca2+ transient in both control and diabetic myocytes at all stimulus
frequencies examined. The degree of potentiation of the Ca2+ transient decr
eased with increasing stimulus frequency in control cells but not in diabet
ic cells. In the absence of taurine the decay of the Ca2+ transient was sig
nificantly slower in diabetic than control myocytes. Taurine was without si
gnificant 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 ca
rdiac myocytes. In addition several of the effects of taurine appeared to b
e more pronounced in diabetic than control cells.