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The role of adenosine A(1) receptors in the ATP-evoked Ca2+ response in rat thyroid FRTL-5 cells
Tekijät: Vainio M, Tornquist K
Kustantaja: ELSEVIER SCIENCE BV
Julkaisuvuosi: 2000
Lehti:: European Journal of Pharmacology
Tietokannassa oleva lehden nimi: EUROPEAN JOURNAL OF PHARMACOLOGY
Lehden akronyymi: EUR J PHARMACOL
Vuosikerta: 390
Numero: 1-2
Aloitussivu: 43
Lopetussivu: 50
Sivujen määrä: 8
ISSN: 0014-2999
DOI: https://doi.org/10.1016/S0014-2999(00)00031-5
Tiivistelmä
The effect of adenosine A(1) receptor activation on the ATP-induced increase in intracellular free Ca2+ was studied in control and protein kinase C down-regulated Fisher rat thyroid (FRTL-5) cells. Long-term phorbol ester treatment, which leads to protein kinase C down-regulation, enhanced the ATP-evoked extracellular Ca2+ influx. The increased Ca2+ influx was antagonized by the adenosine A(1) receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthine (DPCPX). [H-3]DPCPX binding studies revealed that phorbol ester-treatment increased the number of adenosine A(1) receptors. The adenosine A(1) receptor-mediated inhibition of the cyclic AMP formation was not affected by the increased receptor number. We conclude that the enhanced ATP-evoked Ca2+ influx in protein kinase C down-regulated cells is mediated by adenosine formed by hydrolysis of ATP, and that this adenosine interacts with the increased number of A(1) receptors. The mechanism by which adenosine enhances Ca2+ entry is not known. Thus, the larger number of adenosine A(1) receptors broadens the spectrum of adenosine A(1) receptor affected signaling systems in FRTL-5 cells. (C) 2000 Elsevier Science B.V. All rights reserved.
The effect of adenosine A(1) receptor activation on the ATP-induced increase in intracellular free Ca2+ was studied in control and protein kinase C down-regulated Fisher rat thyroid (FRTL-5) cells. Long-term phorbol ester treatment, which leads to protein kinase C down-regulation, enhanced the ATP-evoked extracellular Ca2+ influx. The increased Ca2+ influx was antagonized by the adenosine A(1) receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthine (DPCPX). [H-3]DPCPX binding studies revealed that phorbol ester-treatment increased the number of adenosine A(1) receptors. The adenosine A(1) receptor-mediated inhibition of the cyclic AMP formation was not affected by the increased receptor number. We conclude that the enhanced ATP-evoked Ca2+ influx in protein kinase C down-regulated cells is mediated by adenosine formed by hydrolysis of ATP, and that this adenosine interacts with the increased number of A(1) receptors. The mechanism by which adenosine enhances Ca2+ entry is not known. Thus, the larger number of adenosine A(1) receptors broadens the spectrum of adenosine A(1) receptor affected signaling systems in FRTL-5 cells. (C) 2000 Elsevier Science B.V. All rights reserved.
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