Vasopressin and collecting duct intramembranous particle clusters: a dose-response relationship

Harmanci, Mehmet C.; Stern, P; Kachadorian, W. A.; Valtin, Heinz; Discala, Vincent A.

doi:10.1152/ajprenal.1980.239.6.f560

Cited by 37 publications

(32 citation statements)

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“…However, as shown in Figs. 10 and 11, inhibition of membrane retrieval is not produced solely by exposure to cold, but also occurs when transepithelial water flow is reduced to below an apparent threshold. Fig.…”

Section: Discussionmentioning

confidence: 99%

“…A large body of evidence indicates that particle aggregates are closely correlated with or are themselves water channels responsible for the increase in apical membrane water permeability induced by ADH (reviews 8, 9). Freeze-fracture electron microscopy has also revealed that distinctive intramembrane particle structures are closely correlated with ADHinduced permeability changes in the apical membrane of the mammalian collecting duct (10)(11)(12).…”

Section: Introductionmentioning

confidence: 97%

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

Harris¹,

Wade²,

Handler³

1986

J. Clin. Invest.

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Antidiuretic hormone (ADH) increases the osmotic water permeability (P...) oftoad urinary bladder. This increase is believed to be produced by fusion of intracellular vesicles called aggrephores with the granular cell apical plasma membrane. Aggrephores contain intramembrane particle aggregates postulated to be water channels. ADH-stimulated P.3 is decreased by osmotic gradient exposure, which is termed flux inhibition. We studied flux inhibition by exposing ADH-stimulated bladders to various osmotic gradients. Osmotic water flow was initially proportional to the applied osmotic gradient, but P.., decreased with time. Ultrastructural and quantitative studies of endocytosis demonstrate that apical membrane retrieval was a direct function of the transepithelial osmotic gradient. PO. remained unchanged when apical membrane retrieval was blocked by incubation of bladders at 20C, or under low water-flow conditions. These effects were reversed by increases in temperature or the applied osmotic gradient. We conclude that apical membrane retrieval causes the phenomenon of flux inhibition.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

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

Harris¹,

Wade²,

Handler³

1986

J. Clin. Invest.

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“…When ADH is withdrawn, particle aggregates and aggrephores are retrieved from the apical membrane (9,10), and the water permeability response reverses. The particle aggregates are intimately involved in water permeability (11)(12)(13)(14) and they may well be the site of specific water channels (reviewed in refs. 15 and 16).…”

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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“…On the basis of earlier evidence from amphibian model systems, isolated perfused collecting ducts, and in vivo studies, it was proposed that VP acted by stimulating water channel insertion into the apical plasma membrane by VP-induced exocytosis of cytoplasmic vesicles (29,45,48,57,100,141). While a modeling study in 1993 proposed that both the exocytotic and the endocytotic arms of the pathway were likely to be involved in the process leading to membrane accumulation of water channels (64), most attention was focused on the exocytotic pathway as the main regulatory event in the onset of VP action (141).…”

Section: Role Of Both Exocytosis and Endocytosis In Aqp2 Membrane Accmentioning

confidence: 99%

New insights into the dynamic regulation of water and acid-base balance by renal epithelial cells

Brown

Bouley

Păunescu

et al. 2012

American Journal of Physiology-Cell Physiology

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Maintaining tight control over body fluid and acid-base homeostasis is essential for human health and is a major function of the kidney. The collecting duct is a mosaic of two cell populations that are highly specialized to perform these two distinct processes. The antidiuretic hormone vasopressin (VP) and its receptor, the V2R, play a central role in regulating the urinary concentrating mechanism by stimulating accumulation of the aquaporin 2 (AQP2) water channel in the apical membrane of collecting duct principal cells. This increases epithelial water permeability and allows osmotic water reabsorption to occur. An understanding of the basic cell biology/physiology of AQP2 regulation and trafficking has informed the development of new potential treatments for diseases such as nephrogenic diabetes insipidus, in which the VP/V2R/AQP2 signaling axis is defective. Tubule acidification due to the activation of intercalated cells is also critical to organ function, and defects lead to several pathological conditions in humans. Therefore, it is important to understand how these "professional" proton-secreting cells respond to environmental and cellular cues. Using epididymal proton-secreting cells as a model system, we identified the soluble adenylate cyclase (sAC) as a sensor that detects luminal bicarbonate and activates the vacuolar proton-pumping ATPase (V-ATPase) via cAMP to regulate tubular pH. Renal intercalated cells also express sAC and respond to cAMP by increasing proton secretion, supporting the hypothesis that sAC could function as a luminal sensor in renal tubules to regulate acid-base balance. This review summarizes recent advances in our understanding of these fundamental processes. aquaporin 2; vacuolar ATPase; intercalated cell; principal cell; kidney; epididymis IT HAS BEEN KNOWN FOR MANY years that the major functions of collecting duct principal cells and intercalated cells (Fig. 1) can be regulated by the recycling of aquaporin 2 (AQP2) and the vacuolar H ϩ -ATPase (V-ATPase), respectively, between cytoplasmic vesicles and the plasma membrane (1,26,28,40,54,67,85,142). A considerable amount of the earlier data illuminating these processes was generated using readily accessible model epithelial systems such as the toad urinary bladder (48,83,140) and the turtle bladder (3,127,128), in which cellular function and morphology could be correlated with measurements of water flux and acid-base transport. More recently, a variety of in vitro cell culture models have replaced the toad bladder as an experimental system for water channel trafficking and function. This review will show how cell cultures have provided novel and important information on aquaporin 2 trafficking that has been translatable to the in vivo situation and has allowed the development of strategies to bypass the vasopressin (VP)/vasopressin type 2 receptor (V2R) signaling axis that is defective in nephrogenic diabetes insipidus (NDI). We will go on to demonstrate how the epididymis and vas deferens (from the male reproductive tract) ha...

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Vasopressin and collecting duct intramembranous particle clusters: a dose-response relationship

Cited by 37 publications

References 0 publications

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

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

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

New insights into the dynamic regulation of water and acid-base balance by renal epithelial cells

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