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J Physiol. 2002 Feb 1;538(Pt 3):891-9.

Coupling of vasopressin-induced intracellular Ca2+ mobilization and apical exocytosis in perfused rat kidney collecting duct.

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Department of Physiology and Biophysics, College of Medicine, University of South Florida, Tampa, FL 33612, USA.


Arginine vasopressin (AVP) regulates the osmotic water permeability of the kidney collecting duct by inducing exocytotic insertion of aquaporin-2 into apical membrane. The coupling between AVP-induced intracellular Ca2+ mobilization and apical exocytosis was investigated in isolated perfused rat inner medullary collecting duct (IMCD) segments using confocal fluorescence microscopy. Changes of [Ca2+]i in IMCD cells were measured with fluo-4. A novel confocal imaging technique using a styryl dye, FM1-43, was developed to monitor real-time exocytosis induced by arginine vasopressin. AVP (0.1 nM) triggered a rapid increase of [Ca2+]i in IMCD cells, followed by sustained oscillations. Ratiometric measurement of [Ca2+]i confirmed that the observed [Ca2+]i oscillation was a primary event and was not secondary to changes in cell volume. The frequencies of [Ca2+]i oscillations in each IMCD cell were independent and time variant. 1-Deamino-8-D-arginine vasopressin (a V2 receptor agonist, 0.1 nM) simulated the effects of AVP by triggering [Ca2+]i oscillations. In the absence of extracellular Ca2+, ryanodine (0.1 mM) inhibited AVP-induced Ca2+ mobilization. AVP (0.1 nM) triggered accumulative apical exocytosis in IMCD cells within 20 s after application. Pre-incubating the IMCD with an intracellular Ca2+ chelator, BAPTA, prevented AVP-induced intracellular Ca2+ mobilization, apical exocytosis, and increase of osmotic water permeability. These results indicate that AVP, via the V2 receptor, triggers a calcium signalling cascade observed as [Ca2+]i oscillations in the IMCD and that intracellular Ca2+ mobilization is required for exocytotic insertion of aquaporin-2.

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