Abstract
The key player in proximal tubular Pi reabsorption, the type IIa Na(+)/Pi co-transporter, is internalized upon PTH treatment and degraded in the lysosomes. PTH action is initiated by apically and basolaterally localized PTH receptors, whereby apical effects are most probably via cAMP-independent (via PKC) and basolateral effects via cAMP-dependent (via PKA) regulatory mechanisms. The molecular determinants at the level of the transporter protein or at the level of interacting (regulatory) proteins are not yet known.
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