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1 Departments of Internal Medicine, Physiology and Neurobiology and Anatomy, University of Utah Health Sciences Center, Salt Lake City, UT, USA; Nephrology Research and GRECC, VA Salt Lake City Health Care System, Salt Lake City, UT, USA
2 Department Obstetrics and Gynecology, University of Cincinnati College of Medicine, Cincinnati, OH, USA
* To whom correspondence should be addressed. E-mail: Bellamkonda.Kishore{at}hsc.utah.edu.
Extracellular nucleotides, acting through P2Y2 receptor and the associated phosphoinositide-calcium signaling pathway, inhibit arginine vasopressin (AVP)-stimulated osmotic water permeability in rat inner medullary collecting duct (IMCD). Since a rise in intracellular calcium is frequently associated with enhanced arachidonic acid metabolism, we examined the effect of activation of P2Y2 receptor on the release of prostaglandin E2 (PGE2) in freshly prepared rat IMCD suspensions. Unstimulated IMCD released moderate, but significant amounts of PGE2, which were more sensitive to COX-2 inhibition as compared to COX-1 inhibition. Agonist activation of P2Y2 receptor by ATP
S resulted in enhanced release of PGE2 from IMCD in a time- and concentration-dependent fashion. The purinergic-stimulated release of PGE2 was completely blocked by non-specific COX inhibitors (Flurbiprofen and APHS). Differential COX inhibition studies revealed that purinergic-stimulated release of PGE2 was more sensitive to the COX-1 specific inhibitor (Valeroyl Salicylate) as compared to the COX-2 inhibitor (NS-398). Thus, purinergic stimulation in the presence of COX-2 inhibitor resulted in significantly more release of PGE2 as compared to that in the presence of the COX-1 inhibitor. In conclusion, assuming that increased release of PGE2 is related to its increased production, our results suggest that purinergic stimulation of IMCD results in enhanced production and release of PGE2, in a COX-1-dependent fashion. Since PGE2 is know to affect transport of water, salt and urea in IMCD, the interaction of purinergic system with prostanoid system in IMCD can modulate the handling of water, salt and urea by IMCD, and thus may constitute a vasopressin-independent regulatory mechanism.
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