Cyclic AMP-Related and Cation-Affected Human Platelet Chloride Transport Regulation

Galila Agam, Micha Aviram, Michaela Zilberman-Kaufman, Aser Rothstein, Avinoam A. Livne

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


Cystic fibrosis has been characterized as a defect in the regulation of cyclic AMP-dependent trans- epithelial chloride transport. The activation of cyclic AMP-dependent protein kinase A by cyclic AMP occurs normally in cystic fibrosis cells, but they fail to transport chloride ions in response to protein kinase A stimulation. Defective chloride secretion and abnormal electrolyte transport occurs in several organs including the lung, sweat glands, intestine and pancreas. The present work was aimed at exploring whether the same or similar regulatory systems are functional in platelets, and if they are altered or deficient in individuals with cystic fibrosis. Chloride transport in platelets from normal subjects and from cystic fibrosis patients was measured by cell sizing techniques where chloride permeability is the limiting factor. In platelets from healthy volunteers, the chloride channel blocker, 5-nitro-2-(3-phenylpropylamino) benzoic acid, inhibits the transport in a dose-dependent manner. The preservation of chloride transport capability is shown to be dependent upon the presence of either Ca2+ or two divalent cation substitutes, Cd2+or Cu2+. It is also shown that in normal subjects 0.1 μmol/1 prostaglandin Elwhich elevates cyclic AMP 6 times and abolishes platelet aggregation, significantly enhances the rate constant of the transport. Furthermore, in five out of nine cystic fibrosis patients studied, platelet chloride transport did not respond to stimulation by prostaglandin E1.

Original languageEnglish
Pages (from-to)329-336
Number of pages8
JournalClinical Chemistry and Laboratory Medicine
Issue number6
StatePublished - 1 Jan 1995

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Biochemistry, medical


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