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Prolactin Increases Cytosolic Free Calcium Concentration in Hepatocytes of Lactating Rats^*

Departamento de Biología Molecular (CSIC-UAM), Universidad Autónoma de Madrid 28049 Madrid, Spain;
Departamento de Bioquimica, Facultad de Quimicas, Universidad Castilla-La Mancha 13071 Ciudad Real, Spain

Address all correspondence and requests for reprints to: Dr. J. P. Garcia-Ruiz, Departamento de Biologia Molecular, Facultad de Ciencias, Universidad Autonoma de Madrid, 28049 Madrid, Spain.

Abstract

PRL at a physiological concentration (10^–8 M) produced a very rapid and transient increase in ⁴⁵Ca efflux in freshly isolated hepatocytes, which reached the highest value within 5 min and returned to baseline level after 20 min. PRLinduced ⁴⁵Ca²⁺ efflux resulted in a loss of 15% of total cell calcium, which was similar to that found in vasopressin-treated cells. However, in contrast with the PRL effect, ⁴⁵Ca²⁺ efflux induced by vasopressin was sustained. We demonstrate by using two different approaches, glycogen phosphorylase-a activation and direct cytosolic calcium concentration ([Ca²⁺]_i) measurements, that PRL elicits a ([Ca²⁺]_i) increase. The treatment of hepatic cells with PRL caused a 4-fold stimulation in glycogen phosphorylase-a activity after 2 min of PRL addition. Direct ([Ca²⁺]_i) determination in fluo-3-loaded hepatocytes showed a 11% increase after 5 min of PRL addition. Similar data were observed in hepatocytes stimulated either with vasopressin (10^–7 M) or calcium ionophore A23187 (200 nM). The increase in ([Ca²⁺]_i) promoted by PRL was independent of extracellular calcium or voltage-operated calcium channels. The data demonstrate that calcium is involved in the intracellular signaling of PRL in liver cells and that PRL initiates its action by a Ca²⁺ mobilization from the intracellular stores. (Endocrinology 129: 2857–2861,1991)

Footnotes

^* This work was supported by a grant from Programa Sectorial de Promotion General del Conocimiento and a grant from the Ramon Areces Foundation.

Received June 10, 1991.

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