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1 Department of Physiology and Biophysics, University of Southern California School of Medicine, Los Angeles, California 90033; and 2 Department of Medical Physiology, The Panum Institute, DK-2200 Copenhagen N, Denmark
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 · min1
for 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 membranes to higher
density fractions containing intracellular membrane markers, and
basolateral Na-K-ATPase activity decreased 25%.
[Nle8,18,Tyr34]PTH-(3-34)
failed to increase V or CLi or to
provoke redistribution of NHE3 or NaPi2, but it did inhibit Na-K-ATPase
activity 25%. We conclude that in vivo PTH stimulates
natriuresis/diuresis associated with internalization of apical NHE3 and
NaPi2 and inhibition of Na-K-ATPase activity, that cAMP-protein kinase
A stimulation is necessary for the natriuresis/diuresis and NHE3 and
NaPi2 internalization, and that Na-K-ATPase inhibition is not secondary
to depressed apical Na+ transport.
sodium-potassium-adenosinetriphosphatase; NHE3; NaPi2; parathyroid hormone-(1-34); membrane trafficking
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