Acidosis inhibits sarcoplasmic reticulum Ca2+ uptake and Ca2+-induced Ca2+ release in intact rat ventricular myocytes, but these effects are compensated by an increase in SR Ca2+ content.
In intact rat ventricular myocytes, acidosis inhibits sarcoplasmic reticulum Ca2+ uptake and release, which is compensated by increased SR Ca2+ content due to elevated cytoplasmic Ca2+.
The effect of acidosis on Ca2+ uptake and release by the sarcoplasmic reticulum (SR) of rat ventricular myocytes has been investigated. Intracellular Ca2+ concentration (Ca2+i) was monitored using fura 2; the L-type Ca2+ current (ICa) was monitored using the perforated patch-clamp technique. Acidosis was produced either by superfusing the cells with an acid solution (intracellular and extracellular acidosis) or by NH4Cl withdrawal (intracellular acidosis). Both types of acidosis increased the amplitude, and slowed the declining phase, of the Ca2+ transient. Application of caffeine produced a rise of Ca2+i, which declined in the continued presence of caffeine; the declining phase was slowed by the acid solution but was unaffected by NH4Cl withdrawal. Acidosis decreased the fraction of the caffeine-induced release that was released by electrical stimulation but had no effect on ICa. It is concluded that acidosis inhibits SR Ca2+ uptake and Ca2+-induced Ca2+ release in intact myocytes but that these effects are compensated by an increase in SR Ca2+ content secondary to a rise in cytoplasmic Ca2+.
Hulme et al. (Tue,) reported a other. Acidosis vs. Baseline/Normal pH was evaluated on Ca2+ uptake and release by the sarcoplasmic reticulum. Acidosis inhibits sarcoplasmic reticulum Ca2+ uptake and Ca2+-induced Ca2+ release in intact rat ventricular myocytes, but these effects are compensated by an increase in SR Ca2+ content.