K. Komukai et al., Compensatory role of CaMKII on I-Ca and SR function during acidosis in ratventricular myocytes, PFLUG ARCH, 442(3), 2001, pp. 353-361
It has been suggested that the activity of Ca2+/calmodulin-dependent protei
n kinase II (CaMKII) increases during acidosis in cardiac muscle. Thus we h
ave investigated the role of CaMKII during acidosis by monitoring intracell
ular Ca2+ (using fura-2) and I-Ca (Using the perforated patch clamp techniq
ue) during acidosis, in the absence and presence of the CaMKII inhibitor KN
-93, in rat isolated ventricular myocytes. In the absence of KN-93, acidosi
s (pH 6.5) increased the amplitude of the fura-2 transient and prolonged it
s decay, but in the presence of KN-93 acidosis did not alter the amplitude
and prolonged the decay more. In the absence of KN-93, acidosis increased t
he amplitude of the caffeine-induced fura-2 transient but did not alter its
amplitude in the presence of KN-93. I-Ca did not change significantly duri
ng acidosis in the absence of KN-93 but decreased during acidosis in the pr
esence of KN-93. These results suggest that activation of CaMKII during aci
dosis helps to compensate for the direct inhibitory effects of acidosis on
sarcoplasmic reticular Ca2+ uptake and I-Ca.