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1 Department of Physiology and Biophysics, University of Southern California Keck School of Medicine, Los Angeles, CA, USA
2 Department of Medical Physiology, Division of Renal and Cardiovascular Resarch, The Panum Institute, University of Copenhagen, Copenhagen, Denmark
* To whom correspondence should be addressed. E-mail: mcdonoug{at}hsc.usc.edu.
Renal parathyroid hormone (PTH) action is often studied at high doses (100 µg PTH.kg-1) that lower mean arterial pressure significantly, albeit transiently, complicating interpretation of studies. Little is known about the effect of acute hypotension on proximal tubule Na+ transporters. This study aimed to determine the effects of acute hypotension, induced by aortic clamp or by high dose PTH (100 µg PTH.kg-1), on renal hemodynamics and proximal tubule NHE3 and NaPi2 distribution. Subcellular distribution was analyzed in renal cortical membranes fractionated on sorbitol density gradients. Aortic clamp-induced acute hypotension (from 100 ±3 mmHg to 78 ± 2 mmHg) provoked a 62% decrease in urine output and a significant decrease in volume flow from the proximal tubule detected as a 66% decrease in endogenous lithium clearance. There was, however, no significant change in GFR or subcellular distribution of NHE3 and NaPi2. In contrast, high dose PTH rapidly (<2 min) decreased arterial blood pressure to 51 ± 3 mmHg, decreased urine output and shifted NHE3 and NaPi2 out of the low density membranes enriched in apical markers. PTH at much lower doses (<1.4 µg.kg-1.h-1) did not change blood pressure and was diuretic. In conclusion, acute hypotension per se increases PT Na+ reabsorption without changing NHE3 or NaPi2 subcellular distribution indicating that trafficking of transporters to the surface is not the likely mechanism; in comparison, hypotension secondary to high dose PTH blocks the primary diuretic effect of PTH but does not inhibit the PTH-stimulated redistribution of NHE3 and NaPi2 to the base of the microvilli.
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