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Rabbit cortical collecting ducts express a novel prostacyclin receptor
R L Hébert1, L Regnier, L N Peterson
1Department of Physiology, Faculty of Medicine, University of Ottawa, Ontario, Canada.
The American Journal of Physiology
|January 1, 1995
Summary
Prostaglandin E2 and prostacyclin agonists inhibit water and sodium reabsorption in rabbit kidneys. They act via distinct receptors, suggesting different signaling pathways for regulating kidney function.
Area of Science:
- Nephrology
- Molecular Pharmacology
- Renal Physiology
Background:
- Prostaglandin E2 (PGE2) inhibits vasopressin-stimulated water and sodium transport in the kidney.
- Prostacyclin (PGI2) also inhibits sodium reabsorption in the cortical collecting duct (CCD).
- Increased intracellular calcium ([Ca2+]i) mediates PGE2's inhibition of sodium reabsorption.
Purpose of the Study:
- To investigate the effect of the PGI2 agonist, Iloprost (ILP), on vasopressin-stimulated water permeability (AVP-Lp) and [Ca2+]i in rabbit CCD.
- To determine if ILP activates different receptors than PGE2.
Main Methods:
- Isolated perfused rabbit cortical collecting duct (CCD) studies.
- Measurement of vasopressin-stimulated water conductivity (AVP-Lp).
- Intracellular calcium ([Ca2+]i) measurements using fura 2.
Main Results:
- Both ILP and PGE2 equipotently inhibited AVP-Lp at 10(-7) M.
- Inhibition of AVP-Lp by ILP and PGE2 was additive, indicating distinct receptor activation.
- ILP and PGE2 independently increased [Ca2+]i, with cross-desensitization patterns suggesting separate receptors.
Conclusions:
- PGI2 inhibits AVP-Lp via a novel IP3 prostacyclin receptor.
- PGI2 increases [Ca2+]i by activating an IP1 prostacyclin receptor.
- PGI2 and PGE2 interact with distinct receptors, with PGI2 unable to activate PGE2 receptors and PGE2 having limited activation of PGI2 receptors.