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The role of the sarcoplasmic reticulum as a Ca²⁺ sink in rat uterine smooth muscle cells

A. V. Shmigol, D. A. Eisner * and Susan Wray

The mechanisms responsible for removing calcium ions from the cytoplasm were investigated in single rat uterine myocytes using indo-1.

Trains of depolarizing voltage-clamp pulses increased [Ca²⁺]_i. The rate of decay of [Ca²⁺]_i was slowed by inhibition of the sarcoplasmic reticulum (SR) Ca²⁺-ATPase with cyclopiazonic acid (CPA). However, if the sarcolemmal Na⁺-Ca²⁺ exchanger and Ca²⁺-ATPase were inhibited then recovery of [Ca²⁺]_i was abolished showing that the SR Ca²⁺-ATPase alone cannot produce decay of [Ca²⁺]_i.

In another series of experiments, Ca²⁺ release from the SR was induced with carbachol in a Ca²⁺-free solution. Under these conditions responses to repeated applications of carbachol could be obtained. In the presence of CPA, however, only the first application was effective. This suggests that the SR Ca²⁺-ATPase sequesters a significant amount of Ca²⁺ into the SR.

CPA slowed the rate of decay of [Ca²⁺]_i following carbachol addition by > 50 %. Again, however, after a brief transient fall, decay was abolished when the Na⁺-Ca²⁺ exchanger and sarcolemmal Ca²⁺-ATPase were inhibited.

These data show that, although the SR Ca²⁺-ATPase contributes to the decay of [Ca²⁺]_i, it cannot function effectively in the absence of Ca²⁺ removal from the cell. These data are discussed in the context of the superficial buffer barrier model in which Ca²⁺ is taken up into the SR and then released very close to sarcolemmal Ca²⁺ extrusion sites, i.e. the SR acting in series with the surface membrane extrusion mechanisms. We also suggest that the amount of filling of the SR influences the rate of Ca²⁺ removal.

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