Vasopressin-elicited Water and Urea Permeabilities are Altered in IMCD in Hypercalcemic Rats
| Title: | Vasopressin-elicited Water and Urea Permeabilities are Altered in IMCD in Hypercalcemic Rats |
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| Authors: | Sands, Jeff M.; Flores, Francisco; Baum, Michelle A.; Brown, Edward M.; Ward, Donald T.; Hebert, M.D., Steven C.; Harris, H. William; Kato, Akihiko |
| Publisher: | American Journal of Physiology |
| Date Published: | May 01, 1998 |
| Reference Number: | 261 |
To investigate how hypercalcemia blunts renal concentrating ability, alterations in basal and arginine vasopressin (AVP)-elicited osmotic water (Pf) and urea (Purea) urea permeabilities were measured in isolated perfused terminal inner medullary collecting ducts (IMCD) from control and chronically hypercalcemic rats after dihydrotachysterol (DHT) (M. Levi, L. Peterson, and T. Berl. Kidney Int. 23: 489-497, 1983) treatment. The IMCD Pf of DHT-treated rats did not increase significantly after AVP and was accompanied by a significant 87 +/- 4% reduction in aquaporin-2 (AQP-2) protein but not mRNA. In contrast, both basal and AVP-elicited IMCD Purea from DHT rats were significantly increased and accompanied by a significant 41 +/- 11% increase in AVP-regulated urea transporter protein content. Immunoblotting with anti-calcium polyvalent cation-sensing receptor protein (CaR) antiserum revealed specific alterations in CaR bands in endosomes purified from the apical membranes of inner medulla of DHT rats. These data are the first detailed analyses of hypercalcemia-induced alterations in AVP-regulated permeabilities and membrane transporters in IMCD. We conclude that selective alterations in IMCD transport occur in hypercalcemia, permitting the body to dispose of excess calcium without forming calcium-containing renal stones.
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- IMCD levels of aquaporin-2 (AQP2) and vasopressin-regulated urea transporter (VRUT), and
- the levels in IMCD water permeability (Pf) and urea permeability (Purea).
They did this by feeding an experimental group of rats dihydrotachysterol (DHT), which brought them to a hypercalcemic state, then analyzing their IMCD Pf and Purea levels and their AQP2 and VRUT levels. The authors compared these findings with a control group of rats who were not treated with DHT.
The authors found that the IMCD Pf of DHT-treated rats did not increase significantly after AVP. This failure to increase Pf was accompanied by a major reduction in the amount of AQP2 found in the IMCD. In contrast, the authors found that IMCD Purea significantly increased in the DHT-treated rats. This increase was accompanied by an increase in VRUT levels.
Also found was evidence to suggest that the calcium polyvalent cation-sensing receptors (CaR) in IMCD may be modified in DHT-treated rats. The authors' work presents evidence for hypercalcemia-induced alterations in AVP regulated Pf and Purea along with changes in AQP2 and VRUT levels. They reason that these selective changes represent a coordinated response by the IMCD to help dispose of the excess calcium in a way that prevents the formation of calcium containing kidney stones.