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- Title
Purinergic P2Y<sub>6</sub> Receptors Induce Ca and CFTR Dependent Cl<sup>-</sup> Secretion in Mouse Trachea.
- Authors
Schreiber, Rainer; Kunzelmann, Karl
- Abstract
In airways Cl- secretion is activated and Na+ absorption is inhibited when P2Y2 receptors are stimulated by ATP or UTP. Both nucleotides are subject to degradation to ADP and UDP by ecto-nucleotidases. Here we show that these metabolites change electrolyte transport by stimulation of P2Y6 receptors in mouse trachea. Immunohistochemistry confirmed luminal and basolateral expression of P2Y 6 receptors. In Ussing chamber experiments luminal ADP, UDP or the P2Y6 receptor agonist INS48823 induced both transient and persistent increase in short circuit currents (ISC). Activation of I SC was inhibited by the P2Y6 receptor blocker PPADS. The transient response was inhibited by DIDS, whereas the persistent I SC was inhibited by glibenclamide and by the protein kinase A (PKA) blocker H-89. Moreover, sustained activation of I SC by luminal UDP was inhibited by blocking basolateral K+ channels with 293B. Possible effects of diphosphates on P2Y1 or adenosine receptors were excluded by the inhibitors MRS2179 and 8-SPT, respectively. Inhibition of amiloride sensitive Na+ absorption was only seen after blocking basolateral K+ channels with 293B. In contrast, Cl- secretion activated by basolateral ADP or UDP was only transient and was blocked by the sk4 K+ channel blocker clotrimazole. In summary, activation of luminal P2Y6 receptors in the airways shifts electrolyte transport towards secretion by increasing intracellular Ca+ and activation of PKA. Copyright © 2005 S. Karger AG, Basel
- Subjects
ADENOSINE triphosphate; NUCLEOTIDES; ADENOSINES; CELL receptors; TRACHEA
- Publication
Cellular Physiology & Biochemistry (Karger AG), 2005, Vol 16, Issue 1-3, p099
- ISSN
1015-8987
- Publication type
Article
- DOI
10.1159/000087736