HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 295/6/F1715    most recent 90311.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Zhang, Y. Articles by Kishore, B. K. Search for Related Content PubMed PubMed Citation Articles by Zhang, Y. Articles by Kishore, B. K.

Potential role of purinergic signaling in urinary concentration in inner medulla: insights from P2Y2 receptor gene knockout mice

Nephrology ¹Service and ²Research, and ³Geriatric Research, Education and Clinical Center, Veterans Affairs Salt Lake City Health Care System, and Departments of ⁴Internal Medicine, ⁵Pediatrics, ⁶Physiology, and ⁷Neurobiology and Anatomy, and ⁸Center on Aging, University of Utah Health Sciences Center, Salt Lake City, Utah; and ⁹Renal Division, Emory University School of Medicine, Atlanta, Georgia

Submitted 15 May 2008 ; accepted in final form 25 September 2008

Osmotic reabsorption of water through aquaporin-2 (AQP2) in the inner medulla is largely dependent on the urea concentration gradients generated by urea transporter (UT) isoforms. Vasopressin (AVP) increases expression of both AQP2 and UT-A isoforms. Activation of the P2Y2 receptor (P2Y2-R) in the medullary collecting duct inhibits AVP-induced water flow. To gain further insights into the overarching effect of purinergic signaling on urinary concentration, we compared the protein abundances of AQP2 and UT-A isoforms between P2Y2-R knockout (KO) and wild-type (WT) mice under basal conditions and following AVP administration. Under basal conditions (a gel diet for 10 days), KO mice concentrated urine to a significantly higher degree, with 1.8-, 1.66-, and 1.29-fold higher protein abundances of AQP2, UT-A1, and UT-A2, respectively, compared with WT, despite comparable circulating AVP levels in both groups. Infusion of 1-desamino-8-D-arginine vasopressin (dDAVP; desmopressin; 1 ng/h sc) for 5 days resulted in 2.14-, 2.6-, and 2.22-fold higher protein abundances of AQP2, AQP3, and UT-A1, respectively, in the inner medullas of KO mice compared with WT mice. In response to acute (45 min) stimulation by AVP (0.2 unit/mouse sc), UT-A1 protein increased by 1.39- and 1.54-fold in WT and KO mice, respectively. These data suggest that genetic deletion of P2Y2-R results in increased abundances of key proteins involved in urinary concentration in the inner medulla, both under basal conditions and following AVP administration. Thus purinergic regulation may play a potential overarching role in balancing the effect of AVP on the urinary concentration mechanism.

collecting duct; arginine vasopressin; aquaporin; urea transporters; extracellular nucleotides

This article has been cited by other articles:

				Y. Zhang, R. D. Nelson, N. G. Carlson, C. D. Kamerath, D. E. Kohan, and B. K. Kishore Potential role of purinergic signaling in lithium-induced nephrogenic diabetes insipidus Am J Physiol Renal Physiol, May 1, 2009; 296(5): F1194 - F1201. [Abstract] [Full Text] [PDF]