Both vasopressin-elicited water and urea permeabilities are altered
in the inner medullary collecting duct present in hypercalcemic
rats..
Sands, Jeff M., Francisco X. Flores, Akihiko Kato, Michelle A. Baum,
Edward M. Brown, Donald T. Ward, Steve C. Hebert, and H. William
Harris.
Renal Division, Emory University School of Medicine, Atlanta,
Georgia 30322; Division of Nephrology, Children's Hospital, Boston,
Massachusetts 02115; Endocrine-Hypertension Division, Department of
Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115.
Renal Division, Vanderbilt University School of Medicine, Nashville,
TN 37215
APStracts 5:0036F, 1998.
To investigate how hypercalcemia blunts renal concentrating ability,
alterations in basal and AVP-elicited water (Pf) and urea (Purea)
permeabilities were measured in isolated perfused terminal inner
medullary collecting ducts (IMCD) from control and chronically
hypercalcemic rats after dihydrotachysterol (DHT) (Levi et al. Kidney
Inter. 23:489, 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 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 (VRUT) protein content.
Immunoblotting with anti-calcium/polyvalent cation-sensing receptor
protein (CaR) antiserum revealed specific alterations in CaR bands s
in endosomes purified from the apical membranes of inner medullae 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 occurs in hypercalcemia permitting the body to
dispose of excess calcium without forming calcium-containing renal
stones.
Received 22 October 1997; accepted in final form 6 February 1998.
APS Manuscript Number F337-7.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 19 February 1998