In vivo PTH provokes apical NHE3 and NaPi2 redistribution and Na-K-ATPase inhibition

The aim of this study was to test the hypothesis that in vivo administration of parathyroid hormone (PTH) provokes diuresis/natriuresis through redistribution of proximal tubule apical sodium cotransporters (NHE3 and NaPi2) to internal stores and inhibition of basolateral Na-K-ATPase activity and to determine whether the same cellular signals drive the changes in apical and basolateral transporters. PTH-(1–34) (20 U), which couples to adenylate cyclase (AC), phospholipase C (PLC), and phospholipase A2(PLA2), or [Nle8,18,Tyr34]PTH-(3–34) (10 U), which couples to PLC and PLA2 but not AC, were given to anesthetized rats as an intravenous bolus followed by low-dose infusion (1 U ⋅ kg−1 ⋅ min−1for 1 h). Renal cortex membranes were fractionated on sorbitol density gradients. PTH-(1–34) increased urinary cAMP excretion 3-fold, urine output (V) 2.0 ± 0.1-fold, and lithium clearance (CLi) 2.8 ± 0.3-fold. With this diuresis/natriuresis, 25% of NHE3 and 18% of NaPi2 immunoreactivity redistributed from apical membran...