TY - JOUR
T1 - Properties of voltage-activated [Ca2+](i) transients in single smooth muscle cells isolated from pregnant rat uterus
AU - Shmigol, A. V.
AU - Eisner, D. A.
AU - Wray, Susan
PY - 1998/9/15
Y1 - 1998/9/15
N2 - 1. The intracellular calcium concentration ([Ca2+](i)) was measured at 35°C using the fluorescent indicator indo-1 in patch-clamped, single uterine myocytes from pregnant rats to investigate the relationship between depolarization, Ca2+ current (I(Ca)) and [Ca2+](i). 2. Membrane depolarization activated I(Ca) and produced a [Ca2+](i) transient. The rapid increase in [Ca2+](i) occurred at the same time as the inward I(Ca). Both I(Ca) and the increase in [Ca2+](i) were abolished by nifedipine (10 μM). 3. When the membrane potential was held at -80 mV the threshold depolarization for an increase in [Ca2+](i) was about -55 to -50 mV. As the magnitude of the depolarization was increased to about 0 mV there was an increase in the size of both I(Ca) and the increase in [Ca2+](i). As the magnitude of tire depolarization was further increased both I(Ca) and the [Ca2+](i) increase declined. 4. When the depolarizing pulses were applied at 3 Hz to mimic normal action potentials then the individual [Ca2+](i) transients did not fully relax and a tetanic rise of [Ca2+](i) was observed. Under these conditions, there was not a simple relationship between the magnitude of the Ca2+ response and Ca2+ entry. When pairs of depolarizing pulses were applied, the increase in [Ca2+](i) produced by the second pulse was larger (in relation to the magnitude of the L-type Ca2+ current) than that produced by the first pulse. This facilitation was abolished by both ryanodine and cyclopiazonic acid suggesting a role for release from intracellular stores. 5. We conclude that the L-type Ca2+ current is the major source of Ca2+ ions entering the cell to produce the [Ca2+](i) transient on depolarization. The magnitude of the increase in [Ca2+](i) may, however, be amplified by Ca2+-induced Ca2+ release.
AB - 1. The intracellular calcium concentration ([Ca2+](i)) was measured at 35°C using the fluorescent indicator indo-1 in patch-clamped, single uterine myocytes from pregnant rats to investigate the relationship between depolarization, Ca2+ current (I(Ca)) and [Ca2+](i). 2. Membrane depolarization activated I(Ca) and produced a [Ca2+](i) transient. The rapid increase in [Ca2+](i) occurred at the same time as the inward I(Ca). Both I(Ca) and the increase in [Ca2+](i) were abolished by nifedipine (10 μM). 3. When the membrane potential was held at -80 mV the threshold depolarization for an increase in [Ca2+](i) was about -55 to -50 mV. As the magnitude of the depolarization was increased to about 0 mV there was an increase in the size of both I(Ca) and the increase in [Ca2+](i). As the magnitude of tire depolarization was further increased both I(Ca) and the [Ca2+](i) increase declined. 4. When the depolarizing pulses were applied at 3 Hz to mimic normal action potentials then the individual [Ca2+](i) transients did not fully relax and a tetanic rise of [Ca2+](i) was observed. Under these conditions, there was not a simple relationship between the magnitude of the Ca2+ response and Ca2+ entry. When pairs of depolarizing pulses were applied, the increase in [Ca2+](i) produced by the second pulse was larger (in relation to the magnitude of the L-type Ca2+ current) than that produced by the first pulse. This facilitation was abolished by both ryanodine and cyclopiazonic acid suggesting a role for release from intracellular stores. 5. We conclude that the L-type Ca2+ current is the major source of Ca2+ ions entering the cell to produce the [Ca2+](i) transient on depolarization. The magnitude of the increase in [Ca2+](i) may, however, be amplified by Ca2+-induced Ca2+ release.
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U2 - 10.1111/j.1469-7793.1998.803bg.x
DO - 10.1111/j.1469-7793.1998.803bg.x
M3 - Article
C2 - 9714861
AN - SCOPUS:0032530661
SN - 0022-3751
VL - 511
SP - 803
EP - 811
JO - Journal of Physiology
JF - Journal of Physiology
IS - 3
ER -