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Purinergic receptors in mouse and rat epididymis : Role of luminal ATP and adenosine in V‐ATPase activation
Author(s) -
Belleannee Clemence,
Da Silva Nicolas,
Shum Winnie,
Breton Sylvie
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.998.37
Subject(s) - purinergic receptor , adenosine , p2y receptor , purinergic signalling , atpase , biology , receptor , apyrase , adenosine receptor , v atpase , adenosine triphosphate , calcium in biology , medicine , microbiology and biotechnology , endocrinology , biochemistry , enzyme , agonist
In the epididymis, V‐ATPase is expressed in clear cells and acidifies the lumen where sperm mature and are stored. We showed that luminal alkaline pH triggers the apical membrane accumulation of V‐ATPase and that this process is calcium‐dependent. However, the link between alkaline pH and intracellular calcium is not completely elucidated. Some purinergic receptors are sensitive to pH, and we examined their expression by RT‐PCR in rat epithelial cells isolated by laser capture microdissection. mRNA transcripts for P1 adenosine receptors (subtypes A1, A2B and A3) and P2 ATP receptors (subtypes P2X1, P2X2, P2X4, P2X11, P2Y1 and P2Y2) were detected. Ecto‐ATPase and alkaline phosphatase were also observed, indicating potential degradation of ATP into adenosine in the epididymal lumen. In vivo perfusion of rat and mouse epididymis showed that both ATP (600µM) and adenosine (300µM) induced apical membrane V‐ATPase recruitment even in the absence of an alkaline pH stimulus. BAPTA‐AM abolished the ATP‐mediated effect, indicating the participation of calcium in this response. These data show that ATP and adenosine are sufficient to cause the accumulation of V‐ATPase in the apical membrane of clear cells. The paracrine activation of purinergic receptors might, therefore, play a significant role in the regulation of proton secretion in the male reproductive tract. This work is supported by NIH grant HD40793.