Transepithelial water flow regulates apical membrane retrieval in antidiuretic hormone-stimulated toad urinary bladder.

Harris, H. W.; Wade, James B.; Handler, Jerome S.

doi:10.1172/jci112630

Cited by 51 publications

(48 citation statements)

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“…The impetus for this study was the observations in toad urinary bladder that a serosal-to-mucosal osmotic gradient stimulated membrane retrieval (20,22). Based on the toad bladder data and the collecting tubule data reported here, we proposed that water flow itself might provide a physical force to influence the targeted movement ofmembranes within a cell.…”

Section: Discussionmentioning

confidence: 83%

“…The interesting observation has been made in a number of laboratories that the presence of a serosal-to-mucosal osmotic gradient (serosal > mucosal osmolality) appears to alter the endocytic phase of membrane cycling in toad urinary bladder (20)(21)(22). A serosal-to-mucosal osmotic gradient both increases the endocytic retrieval of fluid-phase fluorescent markers, and enhances the downregulation ofwater permeability in response to prolonged vasopressin stimulation.…”

mentioning

confidence: 99%

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Transcellular water flow modulates water channel exocytosis and endocytosis in kidney collecting tubule.

Kuwahara

Shi²,

Marumo³

et al. 1991

J. Clin. Invest.

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IntroductionThe regulation of osmotic water permeability (Pf) by vasopressin (VP) in kidney collecting tubule involves the exocytic-endocytic trafficking of vesicles containing water channels between an intracellular compartment and apical plasma membrane. The regulation ofwater permeability in vasopressin (VP)'-sensitive epithelia is thought to involve a cycle of exocytosis and endocytosis where intracellular vesicles containing water channels are inserted into and removed from the cellular apical membrane (1, 2). There is a good correlation between the presence ofapical membrane particle aggregates and transepithelial osmotic water permeability in toad bladder granular cells and kidney collecting tubule cells involved in the hydroosmotic response to vasopressin (3-5). Endosomes isolated from toad urinary bladder that were formed in response to vasopressin contained functional water channels that might be recycled between subcellular and plasma membrane compartments (6).Endosomes containing the vasopressin-sensitive water channel had low urea and proton permeabilities (7), and very high water permeability that was not subject to direct biochemical regulation (8). The signaling mechanism responsible for the modulation of membrane cycling is believed to involve a cAMP-dependent protein kinase and the cell cytoskeleton (9); however, the biochemical and physical factors controlling exocytosis and endocytosis have not been established.In kidney collecting tubule, endocytosis of water channels probably occurs by formation of clathrin-coated pits (10-12); however, little is known about the fate of endocytosed membranes or ofthe mechanism by which intracellular membranes fuse with the apical surface in response to vasopressin addition. Endosomes formed in the papillary collecting tubule from Brattleboro rats contained functional water channels only when the rats had received vasopressin or the V2 agonist DDAVP before endosome isolation (13,14), providing strong evidence for a water channel shuttle mechanism in kidney collecting tubule. The vasopressin-induced endosomes did not acidify in response to ATP, and endocytosed fluid phase markers did not colocalize with lysosomes, raising the interesting possibility that intracellular processing of endosomes containing the vasopressin-sensitive water channel does not involve the conventional endocytotic pathway of progressive acidification (15). In kidney proximal tubule, there is rapid constitutive (hormone-independent) endocytosis that also involves clathrin-coated vesicles (12,16,17). However, in contrast to collecting tubule, endosomes from apical membrane of proximal tubule contain functional water channels and do fuse

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Section: Discussionmentioning

confidence: 83%

mentioning

confidence: 99%

Transcellular water flow modulates water channel exocytosis and endocytosis in kidney collecting tubule.

Kuwahara

Shi²,

Marumo³

et al. 1991

J. Clin. Invest.

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“…ADH stimulation without net osmotic water flow (no osmotic gradient) produces aggrephore fusion without apical membrane retrieval (9,10,26 (27 (Fig. 1B).…”

Section: Lactoperoxidase/glucose Oxidase Iodination Of the Apicalmentioning

confidence: 98%

“…Measurements of potential difference (25) and water flow (26) in iodinated bladders were performed as described.…”

mentioning

confidence: 99%

Identification of specific apical membrane polypeptides associated with the antidiuretic hormone-elicited water permeability increase in the toad urinary bladder.

Harris¹,

Wade²,

Handler³

1988

Proc. Natl. Acad. Sci. U.S.A.

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Antidiuretic hormone (ADH) increases the water permeability of the toad urinary bladder. The increase occurs in the apical plasma membrane of granular cells that line the urinary surface of the bladder and is produced by the insertion of water permeability units that have been identified by freeze-fracture electron microscopy as intramembrane particle aggregates. Under water-impermeable conditions, particle aggregates reside in intracellular vesicles called "aggrephores." In response to ADH, the aggrephores fuse with the apical plasma membrane and render it water permeable. When ADH is removed, intramembrane particle aggregates and aggrephores are retrieved from the apical membrane, and it returns to a water-impermeable state. To identify proteins involved in the water permeability response, we used lactoperoxidase/glucose oxidase to "MI-label external apical membrane proteins to compare control and ADH-treated bladders. Several polypeptides were consistently labeled in ADH-treated bladders and not in paired controls. After demonstrating that lactoperoxidase behaves as a fluid-phase marker and is sequestered in aggrephore-like vesicles when ADH is withdrawn, we used the technique of Mellman et al. BMl. 86, 712-7221 to label proteins endocytosed when water permeability declines after ADH is withdrawn to test whether the membrane proteins labeled in ADH-treated bladders behaved like particle aggregates. The internalized membranes contained polypeptides of the same molecular weights (55,000, 17,000-14,000, and 7,000) as those labeled on the apical surface of ADH-treated but not control bladders. These polypeptides are evidently involved in the ADH-stimulated water permeability response and may be components of particle aggregates.Antidiuretic hormone (ADH) plays a major role in the control of water balance of many vertebrates. It stimulates the conversion of specific water-impermeable epithelia to a state of high water permeability. For example, the water permeability of the urinary bladder of the toad Bufo marinus increases by >50-fold, allowing water to flow from dilute urine to blood (1). The purpose of this study was to identify membrane proteins involved in the water permeability change that occurs in the toad bladder in response to ADH.The apical plasma membranes of granular cells form >90o of the bladder surface area in contact with urine, and it is these apical membranes that undergo the remarkable change in water permeability (2). Under basal conditions, the apical cytoplasm of granular cells contains tubularshaped vesicles that have been named "aggrephores" because on freeze-fracture electron microscopy they contain distinctive particle aggregates within their limiting membranes (3-5). Aggrephores store and shuttle particle aggregates into and out of the apical plasma membrane in response to changes in the concentration of ADH (6). In response to ADH, aggrephores fuse with the apical plasma membrane and the plasma membrane becomes enriched in particle aggregates (4-8). When ADH is withdrawn, parti...

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“…This conclusion is based on data showing that (a) there is no luminal acidification of WCV in vitro after addition of ATP (26,27,34), (b) measurements of these vesicles in situ using the 342,4-dinitroanilino)-3'-amino-n-methyldipropylamine (DAMP) method show their lumens are not acidic (6), and (c) immunoblots of purified WCV proteins with anti-proton pump antisera reveal these vesicles do not contain the major subunits of the H' ATPase necessary for activity (35). Factors that modulate retrieval of water channels include ADH removal (6,18,20), the magnitude of a transepithelial osmotic gradient (22,27,36), and cytoplasmic dilution or cell swelling (37). Water channel vesicle endocytosis has recently been associated with changes in the phosphorylation state ofa vesicle-associated 1 5.5-kD protein (38).…”

Section: Vesicles Deliver and Remove Adh Water Channels From The Apicmentioning

confidence: 99%

Current understanding of the cellular biology and molecular structure of the antidiuretic hormone-stimulated water transport pathway.

Harris

Strange²,

Zeidel³

1991

J. Clin. Invest.

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Transepithelial water flow regulates apical membrane retrieval in antidiuretic hormone-stimulated toad urinary bladder.

Cited by 51 publications

References 45 publications

Transcellular water flow modulates water channel exocytosis and endocytosis in kidney collecting tubule.

Transcellular water flow modulates water channel exocytosis and endocytosis in kidney collecting tubule.

Identification of specific apical membrane polypeptides associated with the antidiuretic hormone-elicited water permeability increase in the toad urinary bladder.

Current understanding of the cellular biology and molecular structure of the antidiuretic hormone-stimulated water transport pathway.

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