Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/44452
Title: Effect of P<inf>2Y</inf>Agonists on Adenosine Transport in Cultured Chromaffin Cells
Authors: Sen, Raquel P.
Delicado, Esmerilda G.
Castro López-Tarruella, Enrique 
Miras‐Portugal, M. Teresa
UNESCO Clasification: 32 Ciencias médicas
Keywords: Adenosine transport
Chromaffin cells
Diadenosine tetraphosphates
Nucleoside transport
P2y agonists, et al
Issue Date: 1993
Publisher: 0022-3042
Journal: Journal of Neurochemistry 
Abstract: Adenosine transport in cultured chromaffin cells was inhibited by purinergic P2y‐receptor agonists without significant changes in the affinity constant, the values being between 1 ± 0.4 and 1.6 ± 0.6 μM. The Vmax parameter was modified significantly, being 40 ± 1.0, 26 ± 5.0, 32 ± 3.0, and 22 ± 4.7 pmol/106 cells/min for control, adenosine‐5′‐O‐(2‐thiodiphosphate), 5′‐adenylylimidodiphosphate, and P1,P4‐di(adenosine‐5′‐) tetraphosphate (Ap4A) (100 μM for every effector), respectively. Ap4A, a physiological ligand for P2y receptors in chromaffin cells, showed the highest inhibitory effect (45%). This transport inhibition is explained by an increase in the cytosolic Ca2+ concentration ([Ca2+]i) and the activation of protein kinase C (PKC). Experiments of [Ca2+]i measurement with the fura‐2 technique showed that P2y agonists, as well as bradykinin, were able to increase [Ca2+]i, this effect being independent of the presence of extracellular Ca2+. The peptide bradykinin, determined to be coupled to phosphatidylinositol hydrolysis and internal Ca2+ mobilization in chromaffin cells, exhibited a behavior similar to that of P2y agonists in adenosine transport inhibition (39%). P2y agonists and bradykinin increased PKC activity associated with the membrane fraction (about 50% increase in particulate PKC activity with respect to controls). The present studies suggest that adenosine transport is regulated by P2y‐purinergic receptors mediated via Ca2+ mobilization and PKC activation.
URI: http://hdl.handle.net/10553/44452
ISSN: 0022-3042
DOI: 10.1111/j.1471-4159.1993.tb03192.x
Source: Journal of Neurochemistry [ISSN 0022-3042], v. 60, p. 613-619
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