RELATIONSHIP BETWEEN CALCIUM CURRENT AND CYTOSOLIC CALCIUM IN CANINE GASTRIC SMOOTH-MUSCLE CELLS

We measured free intracellular Ca2+ concentration ([Ca2+]i) and Ca2+ current (I(Ca)) simultaneously in voltage-clamped, indo-1-loaded smooth muscle cells isolated from the circular layer of the canine antrum. Resting [Ca2+]i averaged 144 +/- 20 nM in cells held at -70 mV. Depolarization positive to -50 mV elicited I(Ca) and increased [Ca2+]i. Peak [Ca2+]i occurred between 0 and +10 mV and averaged 372 +/- 48 nM. On repolarization, [Ca2+]i decreased slowly (time constant 2-3 s) and the rate depended on the magnitude of [Ca2+]i. Cells were also voltage clamped with protocols that mimicked the upstroke and plateau phases of slow waves. With simulated plateau potentials of -55 to -45 mV, [Ca2+]i increased transiently as a result of the small transient I(Ca) elicited by the upstroke depolarization. Sustained I(Ca) was of sufficient magnitude with plateau depolarizations positive to -40 mV to cause a secondary rise in [Ca2+]i throughout the plateau phase. These data suggest that at the plateau potential of slow waves in situ, I(Ca) is sufficient to cause a sustained increase in [Ca2+]i. The resulting accumulation of Ca2+ may couple the slow wave plateau to contraction and may increase the open probability of Ca2+ -activated K channels. The latter may provide the outward current necessary to initiate repolarization.