Role of the cytoskeleton in the control of transcellular water flow by vasopressin in amphibian urinary bladder

Pearl, M.; Taylor, Ann

doi:10.1111/j.1768-322x.1985.tb00421.x

Cited by 42 publications

(23 citation statements)

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“…If this is true, then microtubules might function as "tracks" on which the aggrephores are moved to the apical membrane by molecular motors such as dynein or kinesin (reviewed in Vale [45]). In support of this hypothesis, several investigators have shown that inhibitors ofdynein ATPase activity also inhibit ADH-sensitive water flow (44).…”

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

confidence: 80%

“…A good deal of indirect evidence, however, has implicated the cytoskeleton in this process. Numerous studies using colchicine, cytochalasin B, and thin-section electron microscopy suggest that both microtubules and microfilaments participate in vesicle-mediated particle aggregate insertion and removal (reviewed in Pearl and Taylor [44]). Their exact roles however remain to be determined.…”

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

confidence: 99%

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

Harris

Strange²,

Zeidel³

1991

J. Clin. Invest.

112

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

confidence: 80%

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.

112

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“…Disruption of the actin cytoskeleton inhibits and antidiuretic hormone-induced increase in water permeability in toad urinary bladder and other tissues (Pearl & Taylor, 1985). Less is known about its role in solute transport but disruption of the cytoskeleton with cytochalasins reduced volume regulation in Necturus gall-bladder (Foskett & Spring, 1985) and rabbit proximal tubules (Linshaw, 1989), probably by mechanisms which prevented the activation of KCl transport out of the cells.…”

Section: Discussionmentioning

confidence: 99%

Sodium‐dependent regulation of epithelial sodium channel densities in frog skin; a role for the cytoskeleton.

Chou

1993

The Journal of Physiology

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SUMMARY1. A weak electroneutral sodium channel blocker 6-chloro-3,5-diamino-pyrazine-2-carboxamide was used to perform noise analysis on isolated epithelium from Rana fuscigula to determine the cellular mechanism underlying autoregulation of Na+ channel densities in response to a reduction in the mucosal Na+ concentration.2. The inherent transport rates of these tissues were generally lower than in other frog skins. and to a lesser extent by an increase in NT, the total number of open and closed channels. 5. We also examined the role of the cytoskeleton in the regulation of Na+ channel densities. Colchicine treatment, which disrupted microtubules, had no apparent effect on the ability of the tissues to autoregulate their Na+ channel densities.6. The integrity of the microfilaments were essential for autoregulatory changes in No. After we had disrupted the microfilaments with cytochalasin B, we observed a marked reduction in the ability of the tissues to increase N0. 7. The mean No did not increase in response to a drop in mucosal Na+ despite the fact that /3' increased by 69 %. We, therefore, assumed that cytochalasin B did not affect Na+ channels already present in the membrane but interfered with recruitment of new channels. Significantly, we did not observe any increase in NT. 8. In kidney and other tight epithelia, microfilaments are responsible for regulating the delivery of newly synthesized membrane proteins. We believe that our results with cytochalasin-treated tissues support the theory that autoregulatory changes in N0 are also regulated by the recruitment of channels from a cytoplasmic pool.

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“…The results are summarized in Table 2. The development of NEM-induced water flow was inhibited when the serosal bath was acidified to pH 6 5, and following exposure of bladders to (a) the metabolic inhibitor iodoacetate, (b) quinidine (a drug known to increase cytosolic free calcium (Lorenzen, Lee & Windhager, 1984)), (c) the cytoskeleton-active drugs nocodazole (which disrupts microtubules), cytochalasins B and D (which disrupt microfilaments), or EHNA (an inhibitor of dynein) (Pearl & Taylor, 1985), (d) cationized ferritin (which is believed to inhibit the response to vasopressin by stimulating the endocytic retrieval of water channels Hemibladders were pre-incubated at low pH or with an inhibitor under the conditions shown, prior to stimulation with 0 1 mm mucosal NEM. Paired controls were stimulated with NEM without exposure to low pH or inhibitor.…”

Section: Horseradish Peroxidase Labellingmentioning

confidence: 99%

“…The hydrosmotic response to the hormone is mediated by cyclic adenosine 3',5'-monophosphate (cAMP), is energy requiring (Handler, Petersen & Orloff, 1966), and is dependent on the integrity of microtubules and microfilaments (Pearl & Taylor, 1985). The increase in water permeability is caused by the exocytotic insertion of specific water channels into the apical plasma membrane of the granular cells.…”

Section: Introductionmentioning

confidence: 99%

Activation of the vasopressin‐sensitive water permeability pathway in the toad bladder by N‐ethyl maleimide

Marples¹,

Bourguet²,

Taylor³

1994

Experimental Physiology

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SUMMARYVasopressin stimulates transepithelial water flow in the toad urinary bladder. We report here that N-ethyl maleimide (NEM) (0-1 mM) produces a similar increase in osmotic water flow when applied to the mucosal surface of the tissue. NEM-induced water flow is sensitive to inhibitors of hormone-induced water flow, including serosal acidification, or exposure to quinidine or cytoskeleton-disruptive drugs. NEM-induced water flow is additive with that induced by a submaximal, but not a maximal, dose of vasopressin. The response to mucosal NEM is not reversed on removal of the reagent, but established NEM-induced water flow can be inhibited by serosal acidification or quinidine. Like vasopressin, mucosal NEM induces the appearance of fusion profiles and intramembranous particle aggregates (putative water channels) in the apical plasma membrane of the granular cells, and the incidence of particle aggregates correlates with water flow. NEM does not cause an increase in intracellular cAMP.Our data suggest that NEM stimulates transepithelial water flow by irreversibly activating cellular mechanisms normally triggered by vasopressin, hence causing the insertion of water channels.

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Role of the cytoskeleton in the control of transcellular water flow by vasopressin in amphibian urinary bladder

Cited by 42 publications

References 0 publications

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

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

Sodium‐dependent regulation of epithelial sodium channel densities in frog skin; a role for the cytoskeleton.

Activation of the vasopressin‐sensitive water permeability pathway in the toad bladder by N‐ethyl maleimide

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