d-609 has been researched along with 9-(tetrahydro-2-furyl)-adenine* in 1 studies
1 other study(ies) available for d-609 and 9-(tetrahydro-2-furyl)-adenine
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Apical and basolateral ATP-induced anion secretion in polarized human airway epithelia.
The present study investigated mechanisms underlying apical and basolateral P2Y(1)-mediated Cl(-) secretion in human airway epithelial cells. Apical and basolateral ATP induced short-circuit currents (I(sc)) with different properties via P2Y(1) receptors. The former comprised an immediate rise followed by a slow attenuation, whereas the latter was a transient rise with a higher peak and shorter duration (< 2 min). The actions of ATP were simulated by those of ADP, ADPbetaS, and ATPgammaS. Antagonists of phosphatidylinositol-phospholipase C (U73122, ET-18-OCH(3)) were without any effect on the bilateral ATP-induced I(sc), which were, in contrast, attenuated by a phosphatidylcholine-phospholipase C inhibitor (D609) and an adenylate cyclase inhibitor (SQ22536). The responses to ATP from either aspect were also sensitive to an intracellular Ca(2+) chelator, 1,2-bis (o-amino-phenoxy)-ethane-N,N,N',N'-tetraacetic acid tetra-(acetoxymethyl)-ester, or a Ca(2+)-activated K(+) channel inhibitor, charybdotoxin, although differential Ca(2+) signals were concomitant with each reaction. Nystatin permeabilization studies revealed a good correlation between the I(sc) and the basolateral K(+) current rather than the apical Cl(-) current under ATP-stimulated conditions. In conclusion, apical and basolateral P2Y(1) receptors couple with both phosphatidylcholine-phospholipase C and adenylate cyclase, leading to Cl(-) secretion, whose rate is essentially regulated by the Ca(2+)-activated K(+) channel-mediated K(+) conductance. This suggests the importance of this channel in airway mucociliary clearance. Topics: Adenine; Adenosine Triphosphate; Adenylyl Cyclase Inhibitors; Bridged-Ring Compounds; Calcium; Cell Polarity; Charybdotoxin; Chloride Channels; Chlorides; Cystic Fibrosis Transmembrane Conductance Regulator; Electrophysiology; Enzyme Inhibitors; Epithelial Cells; Humans; Lung; Norbornanes; Phosphatidylcholines; Phosphatidylinositols; Phospholipid Ethers; Potassium; Potassium Channels, Calcium-Activated; Receptors, Purinergic P2; Receptors, Purinergic P2Y1; Thiocarbamates; Thiones; Type C Phospholipases | 2004 |