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. 1989 Apr 1;259(1):125–129. doi: 10.1042/bj2590125

Influx of bivalent cations can be independent of receptor stimulation in human endothelial cells.

T J Hallam 1, R Jacob 1, J E Merritt 1
PMCID: PMC1138481  PMID: 2541679

Abstract

Stimulation of human umbilical-vein endothelial cells by agonists such as histamine or thrombin promotes an influx of Ca2+, causing an increase in cytoplasmic free Ca2+ ([Ca2+]i) that is dependent on the continued presence of both agonist and extracellular Ca2+. This influx can also be clearly detected by using Mn2+ as a marker for Ca2+ entry, since Mn2+ quenches fura-2 fluorescence. The internal stores can be discharged in nominally Ca2+-free solution by stimulation for a brief period by 100 microM-histamine, with the stimulation being terminated by addition of 20 microM of the H1 antagonist mepyramine. After this (i.e. in the continuous presence of antagonist) a stimulated bivalent-cation influx can still be detected, as evidenced by the following observations: (a) addition of Mn2+ produces a stimulated quench, (b) addition of Ca2+ produces a transient rise in [Ca2+]i, (c) addition of 1 unit of thrombin/ml produces a much attenuated response unless the cells are exposed for a short period to 1 mM extracellular Ca2+. These results imply that stimulated bivalent-cation influx may be a direct consequence of the discharge of the internal Ca2+ stores rather than a direct consequence of the presence of agonist.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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