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1 Department of Internal Medicine, University of Utah Health Sciences Center, Salt Lake City, UT, USA; Department of Physiology, University of Utah Health Sciences Center, Salt Lake City, UT, USA; Nephrology Research, VA Salt Lake City Health Care System, Salt Lake City, UT, USA
2 Department of Neurobiology and Anatomy, and Geriatric Research, Education, and Clinical Center, University of Utah Health Sciences Center, and VA Salt Lake City Health Care System, Salt Lake City, UT, USA
3 Department of Internal Medicine, University of Utah Health Sciences Center, Salt Lake City, UT, USA; Nephrology Research, VA Salt Lake City Health Care System, Salt Lake City, UT, USA
* To whom correspondence should be addressed. E-mail: Bellamkonda.Kishore{at}hsc.utah.edu.
Circulating vasopressin levels change in hydrated and dehydrated conditions and thus control osmotic water permeability (Pf) of inner medullary collecting duct (IMCD). Prostaglandin E2 (PGE2) antagonizes vasopressin-induced Pf of IMCD. Previously we showed that activation of P2Y2 receptor (P2Y2-R) in IMCD results in production and release of PGE2, and P2Y2-R mRNA and protein are significantly elevated in inner medullae of hydrated rats as compared to dehydrated rats. Therefore, we examined whether the altered expression of P2Y2-R in hydrated and dehydrated states is associated with corresponding changes in P2Y2-R-mediated PGE2 release by the IMCD. Rats were hydrated by providing sucrose-water as the sole drinking fluid, or dehydrated by water deprivation for 2 days. This resulted in high output-low osmolality, and low output-high osmolality urines in hydrated and dehydrated rats, respectively. In hydrated rats, there was a significant increase in tubular fluid PGE2, measured indirectly by assessing the urinary PGE2 metabolite. Stimulation of freshly isolated IMCD preparations in vitro with P2Y2-R agonist (ATPăS) showed a marked increase in the release of PGE2 in hydrated rats as compared to normal rats. These responses were blunted in the IMCD prepared from dehydrated rats. The P2Y2-R-mediated PGE2 release in the IMCD of hydrated rats was mediated largely by COX-1 since COX-1-specific inhibitor valeroyl salicylate completely blocked the release. The COX-2-specific inhibitor has only a modest and insignificant inhibitory effect. In conclusion, the increased sensitivity of purinergic-prostanoid interaction seen in the IMCD of hydrated rats may represent a novel vasopressin-independent regulatory mechanism of IMCD function.
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