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Studies of oxytocin-induced phosphorylation of myosin light chain (MLC), resulting in myometrial contraction, suggest that extracellular Ca(2+) influx is involved in its signal transduction. To explore the possibility that intracellular Ca(2+) mobilization by oxytocin may also contribute to MLC phosphorylation, we investigated the relative contributions of these Ca(2+) sources to oxytocin signal transduction in myometrium of pregnant rat. In pregnant rat myometrium, oxytocin-induced Ca(2+) influx occurs via an L-type voltage-dependent Ca(2+) channel. Treatment with verapamil, an antagonist specific for these channels, significantly diminished MLC phosphorylation observed in response to oxytocin administration without affecting the release of Ca(2+) from intracellular Ca(2+) stores. Furthermore, oxytocin-induced MLC phosphorylation was not observed when extracellular Ca(2+) was not present. Our results clearly indicate that extracellular Ca(2+) influx, rather than release from Ca(2+) storage sites, is essential for oxytocin-induced MLC phosphorylation.

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The effects of oxytocin, PGF_2α and PGE₂ on [Ca²⁺]_i of isolated longitudinal muscle cells of term pregnant rats were investigated using Fura-2. Oxytocin, PGF_2α and PGE₂ induced an initial rapid increase followed by a secondary gradual increase in [Ca²⁺]_i in the presence of 1.5 mM Ca²⁺. The initial maximum increases in [Ca²⁺]_i were obtained at 6 s for oxytocin, 20 s for PGF_2α and 30 s for PGE₂ after addition of the stimulants. The EC₅₀ values obtained from the curves were 2.0 nM for oxytocin, 250 nM for PGF_2α and 2,200 nM for PGE₂. On the other hand, the increases in [Ca²⁺]_i induced by the stimulants were nearly abolished by removal of the extracellular Ca²⁺. The stimulants induced biphasic increases in [Ca²⁺]_i which were highly extracellular Ca²⁺-dependent processes, and the order of potencies for the stimulants was oxytocin » PGF_2α > PGE₂ in terms of affinity as well as magnitude. These results might indicate differences in the weight of the physiological role of the stimulants for regulating uterine contractility.