1: Eur J Biochem 1996 Jun 1;238(2):576-81
Adenosine stimulates calcium influx in isolated rat hepatocytes.
Tinton SA, Chow SC, Buc-Calderon PM, Kass GE
Departement des Sciences Pharmaceutiques, Universite Catholique de Louvain,
Bruxelles, Belgium.
The mechanism of stimulation of Ca2+ entry into hepatocytes by adenosine
was investigated. When Fura-2-loaded hepatocytes were suspended in a nominally
Ca(2+)-free buffer, adenosine produced only a small transient increase
in the cytosolic free Ca2+ concentration ([Ca2+)i). However, on restoration
of an extracellular Ca2+ concentration of 1.3 mM, a rapid increase in [Ca2+]i
occurred, which indicates activation of a Ca(2+)-influx pathway. Adenosine
augmented the rate of Ca2+ influx triggered by maximally effective oncentrations
of thapsigargin or cAMP, but was without effect on the rate of Ca2+ entry
that resulted from phospholipase-C-linked-receptor activation by maximally
effective concentrations of vasopressin or ATP. However, in contrast to
vasopression and ATP, adenosine did not stimulate Mn2+ entry. The rate
of Mn2+ influx after stimulation of the hepatocytes with vasopressin was
not increased by adenosine treatment. The stimulation of hepatocytes with
adenosine did not result in significant accumulation of inositol phosphates
or cAMP. Furthermore, the rate of adenosine-induced Ca2+ entry in hepatocytes
was only slightly reduced in the presence of the P1 purinoceptor antagonist
8-phenyltheophylline. In contrast, the receptor-mediated-Ca(2+)-entry antagonist
SK&F 96365 nearly completely blocked the Ca(2+)-entry response without
any effect on internal-Ca(2+)-pool mobilisation by adenosine. It is concluded
that adenosine activates the internal-pool-regulated pathway of Ca2+ entry
and an additional pathway that appears comparable to the previously reported
receptor-dependent pathway, except that Mn2+ entry is not stimulated.
PMID: 8681974, UI: 96283857