Abstract
Sodium influx in serum-deprived human diploid fibroblasts can be stimulated by addition of serum (5-fold) or the divalent cation ionophore A23187 (3-fold). The possible involvement of calmodulin in serum or A23187 stimulation of Na+ influx has been investigated by using six psychoactive agents that are known to bind calmodulin and inhibit calmodulin-sensitive enzymes. Each agent inhibited serum- and A23187-stimulated Na+ influx in a dose-dependent manner. Furthermore, the K1 for inhibition of serum-stimulated Na+ influx correlates directly with the Ca2+-specific calmodulin binding previously determined in a cell-free system [Levin, R. M. & Weiss, B. (1979) J. Pharmacol. Exp, Ther. 208, 454--459]. None of the agents tested had any effect on the serum-insensitive component of net Na+ influx in these cells. These data support the concept that serum and A23187 stimulate Na+ influx in human diploid fibroblasts via an increase of intracellular Ca2+ and a subsequent calmodulin-mediated activation of the amiloride-sensitive transport pathway.
MeSH Terms
Biological Transport/drug effects
Blood
Calcimycin/antagonists & inhibitors
Calcium-Binding Proteins/physiology
Calmodulin/antagonists & inhibitors,physiology
Cells, Cultured
Culture Media
Humans
Kinetics
Sodium/metabolism
Trifluoperazine/pharmacology
Chemicals
Calcium-Binding Proteins
Calmodulin
Culture Media
Trifluoperazine
Calcimycin
Sodium
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Owen N E
Villereal M L
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