| Summary: | The Pi concentration of CSF is about one‐half that of plasma in mammals, a phenomenon confirmed here in the spiny dogfish, Squalus acanthias . The objective of the present study was to characterize the role of CP in setting CSF [Pi]. The large sheet‐like IVth CP of the shark was mounted in Ussing chambers where unidirectional 33 Pi fluxes revealed potent active transport from CSF to blood (Bl) side under short‐circuited conditions. The flux ratio was 25:1 with an average transepithelial resistance of 91 ± 18.9 Ω × cm 2 and electrical potential difference of +0.9 ± 0.17 mV, CSF side positive. The active Pi absorption from CSF was inhibited by 10 mM arsenate, depolarization with 100 mM K + , 0.2 mM ouabain and by Na + ‐free medium. Li + stimulated transport 2‐fold compard to Na + ‐free medium. Phosphonoformic acid (1 mM) had no effect on active Pi transport. RT‐PCR revealed both PiT1 and PiT2 gene expression, but no NaPiII expression, in the shark CP. PiT2 immunoreactivity was present by immunoblot, and immunohistochemistry localized the PiT2‐like transporter in the CP apical microvillar border. In conclusion, the CP actively removed Pi from the CSF. This process has transport properties consistent with a PiT‐type, Na + ‐dependent transporter. A PiT‐like transporter is localized to the apical microvilli of the CP. Supported by NSF.
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