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Title: The ATP4- receptor-operated channel (P2Z class) of human lymphocytes allows Ba2+ and ethidium+ uptake: inhibition of fluxes by suramin.
Austin Authors: Wiley, J S;Chen, R;Jamieson, Gary P
Affiliation: Haematology Department, Austin Hospital, Heidelberg, Victoria, Australia
Issue Date: 15-Aug-1993
Publication information: Archives of Biochemistry and Biophysics; 305(1): 54-60
Abstract: It is now recognized that extracellular ATP can open a receptor-operated ion channel in a variety of cell types. In human lymphocytes this P2Z purinergic channel conducts Na+, K+, Rb+, Li+, and Ca2+ but its permeability to larger cations is not known. Fluorometric measurements were used to show that ATP4- induced the entry of Sr2+ (87 Da) and Ba2+ (137 Da) into human lymphocytes loaded with fura-2. Flow cytometry was used to show that ATP4- induced the entry of ethidium+ (314 Da) but that the larger propidium2+ cation (414 Da) was excluded. ATP(4-)-induced entry of both Ba2+ and ethidium+ showed features previously demonstrated for smaller cation permeants: (i) inhibition by amiloride analogs, (ii) sigmoid dependence of flux on ATP concentrations, and (iii) inhibition by extracellular Na+ ions. Specific inhibitors of L-type voltage-gated Ca2+ channels (nisoldipine and diltiazem) had no effect on ATP(4-)-induced Ba2+ influx. Suramin and reactive blue 2, which are recognized antagonists of ATP-operated purinergic receptors in other tissues, inhibited ATP-induced uptake of ethidium+ in lymphocytes with K1/2 of 61 and 69 microM, respectively. However, hexamethylene amiloride was a more potent inhibitor of ATP-induced ethidium+ uptake with a K1/2 of 13 microM. These data show that the ATP4- receptor-operated channel of human lymphocytes allows influx of cations as large as Ba2+ or ethidium+ and that this influx is inhibited by suramin and reactive blue 2.
Gov't Doc #: 7688203
DOI: 10.1006/abbi.1993.1392
Type: Journal Article
Subjects: Adenosine Triphosphate.pharmacology
Biological Transport.drug effects
Flow Cytometry
Ion Channels.drug effects.physiology
Leukemia, Lymphocytic, Chronic, B-Cell
Lymphocytes.drug effects.metabolism
Protein Synthesis Inhibitors.pharmacology
Appears in Collections:Journal articles

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