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First published online 26 June 2003
doi: 10.1242/jcs.00640

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The prostaglandin E₂ analogue sulprostone antagonizes vasopressin-induced antidiuresis through activation of Rho

¹ Forschungsinstitut für Molekulare Pharmakologie, Campus Berlin-Buch, Robert-Rössle-Strasse 10, 13125 Berlin, Germany
² Universita de Bari, Dipartimento di Fisiologia Generale e Ambientale, Via Amendola 165/A, 70126 Bari, Italy
³ Freie Universität Berlin, Institut für Pharmakologie, Thielallee 67-73, 14195 Berlin, Germany

^* Author for correspondence (e-mail: klussmann{at}fmp-berlin.de)

Accepted 23 April 2003

Arginine-vasopressin (AVP) facilitates water reabsorption in renal collecting duct principal cells by activation of vasopressin V2 receptors and the subsequent translocation of water channels (aquaporin-2, AQP2) from intracellular vesicles into the plasma membrane. Prostaglandin E₂ (PGE₂) antagonizes AVP-induced water reabsorption; the signaling pathway underlying the diuretic response is not known. Using primary rat inner medullary collecting duct (IMCD) cells, we show that stimulation of prostaglandin EP₃ receptors induced Rho activation and actin polymerization in resting IMCD cells, but did not modify the intracellular localization of AQP2. However, AVP-, dibutyryl cAMP- and forskolin-induced AQP2 translocation was strongly inhibited. This inhibitory effect was independent of increases in cAMP and cytosolic Ca²⁺. In addition, stimulation of EP₃ receptors inhibited the AVP-induced Rho inactivation and the AVP-induced F-actin depolymerization. The data suggest that the signaling pathway underlying the diuretic effects of PGE₂ and probably those of other diuretic agents include cAMP- and Ca²⁺-independent Rho activation and F-actin formation.

Key words: PGE₂, Aquaporin, AQP2, Rho, Vasopressin, Kidney

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