Hs. Choi et al., The effect of acidosis on systolic Ca2+ and sarcoplasmic reticulum calciumcontent in isolated rat ventricular myocytes, J PHYSL LON, 529(3), 2000, pp. 661-668
1.We have investigated the mechanisms responsible for the changes of systol
ic Ca2+ that occur in voltage-clamped rat ventricular myocytes during acido
sis produced by application of the weak acid butyrate (30 mM). Intracellula
r pH regulation was inhibited with dimethylamiloride (bicarbonate-free solu
tion).
2. The application of butyrate produced an intracellular acidification of 0
.33 pH units. This was accompanied by a decrease in systolic Ca2+ to about
50 % of control. However, within 2 min, systolic Ca2+ returned to control l
evels.
3. The decrease in systoIic Ca2+ was accompanied by a decrease in the Na+-C
a2+ exchange current observed on repolarisation so that the calculated Ca2 efflux on Na+-Ca2+ exchange was less than the entry on the L-type Ca2+ cur
rent. The magnitude of the Na+-Ca2+ er;change current recovered along with
systolic Ca2+ until it equalled the Ca2+ entry on the L-type Ca2+ current.
4. From the measurement of Ca2+ fluxes, it was calculated that, during acid
osis, the cell gains 121.6 +/- 16.2 mu mol l(-1) of Ca2+. This is equal to
the measured increase of sarcoplasmic reticulum (SR) calcium content obtain
ed by applying caffeine (20 mM) and integrating the resulting Na+-Ca2+ exch
ange current.
5. We conclude that the recovery of the amplitude of the systolic Ca2+ tran
sient is due to decreased SR calcium release, resulting in reduced Ca2+ eff
lux from the cell leading to increased SR calcium content.