Effects of Vasopressin on Toad Bladder Membrane Proteins: Relationship to Transport of Sodium and Water

Ferguson, D. R.; Twite, B R

doi:10.1677/joe.0.0610501

Cited by 25 publications

(7 citation statements)

References 7 publications

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“…Thus, the sensitivity of the sodium transport response was comparable to that of urea. Water flow was not determined; however, Ferguson and Twite (1974) have reported that sodium transport responds to vasopressin prior to water flow in the toad bladder.…”

Section: Effect Of Vasopressin On Sodium and Urea Transportmentioning

confidence: 99%

Membrane pathways for water and solutes in the toad bladder: I. Independent activation of water and urea transport

et al. 1979

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Vsopressin activates a number of transport systems in the toad bladder, including the systems for water, urea, sodium, and other small solutes. Evidence from experiments with selective inhibitors indicates that these transport systems are to a large extent functionally independent. In the present study, we show that the transport systems can be separately activated. Low concentrations of vasopressin (1 mU/ml) activate urea transport with virtually no effect on water transport. This selective effect is due in part to the relatively greater inhibitor action of endogenous prostaglandins on water transport. Low concentrations of 8-bromoadenosine cyclic AMP, on the other hand, activate water, but not urea transport. In additional experiments, we found that varying the ratio of exogenous cyclic AMP to theophylline activated water or urea transport selectively. These studies support the concept of independently controlled systems for water and solute transport, and provide a basis for the study of individual luminal membrane pathways for water and solutes in the accompanying paper.

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Section: Effect Of Vasopressin On Sodium and Urea Transportmentioning

confidence: 99%

Membrane pathways for water and solutes in the toad bladder: I. Independent activation of water and urea transport

et al. 1979

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“…The nature of the specific changes in the luminal membrane which might explain induced changes in permeability, however, remains unknown. On biochemical grounds protein membrane components have been implicated in vasopressin-induced movement of water, sodium, and urea [9,10,13,31,38]. Although correlated structural evidence for these components has not been reported, recent freeze-fracture observations by Chevalier et al [5] and us [18] may be pertinent.…”

mentioning

confidence: 99%

Membrane structural and functional responses to vasopressin in toad bladder

et al. 1976

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Summary. Freeze-fracture electronmicroscopy demonstrates that vasopressin stimulation of isolated toad bladder results in a striking morphologic alteration of epithelial membrane structure. This alteration is characterized by the aggregation of intramembranous particles in orderly linear arrays at multiple sites in the luminal membranes of granular cells specifically. The size ,of these aggregates varies considerably, in terms of area, over a range from 0.5 to 70x 10 -3 gm 2. The median aggregate size is about 10.5x 10 .3 gm 2. Since the extent of vasopressin-associated particle aggregation, in terms of frequency of sites per area of membrane or cumulative area of membrane occupied by them, closely correlates with induced changes in transport function, as measured by osmotic water flow, the aggregates themselves appear to be of physiologic significance in the mechanism of action of vasopressin. This hypothesis is supported by the observations that sites of aggregation occur (a) in response to serosal exposure to hormone specifically, (b) independently of an osmotic gradient, and (c) following stimulation with cyclic adenosine monophosphate.The isolated toad urinary bladder has been used extensively to investigate the mechanism by which vasopressin acts to enhance the transepithelial movement of water and many solutes, especially sodium and urea. It has been established that the permeability barrier in toad bladder which is altered by vasopressin stimulation to permit this effect on these substances is located within its epithelial luminal membrane [7,14,16,19,22,24]. In addition, considerable evidence indicates that the pathways by which these different substances traverse the luminal barrier are selective and distinct [2,3,12,20,21,27,31,34,39]. In the case of water, the luminal permeability barrier which is altered by vasopressin stimulation appears specifically confined to granular cells [6,8,11,33], but for the other substances comparable information is not available.

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“…used in the present work may be associated with direct permeability effects of the hormone (Snart & Sanyal, 1968). It has been shown to give rise to a maximum stimulation of Na+ transport and an increased 02 consumption (Wright & Snart, 1971 a, b;Ferguson & Twite, 1974). The dose-response characteristic for this physiological effect suggests the presence of an octapeptide hormone receptor with an affinity constant of the order 5 x 108 1./mole (450 i.u.…”

Section: Discussionmentioning

confidence: 82%

“…has previously been associated with direct permeability effects of vasopressin and maximum stimulation of Na+ transport (Snart, 1970) whereas the higher doses of vasopressin (100 mu./ml.) have been associated with maximum stimulation of adenylate cyclase activity (Besley & Snart, 1973) dephosphorylation of membrane proteins and stimulation of water transport (Ferguson & Twite, 1974). METHODS Toad bladder preparation.…”

Section: Introductionmentioning

confidence: 99%

Effect of steroid depletion on the response of toad bladder to vasopressin.

Debnam¹,

Hewitt²,

Snart³

1975

The Journal of Physiology

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1. We have investigated the water transport and short‐circuit current (s.c.c.) response to vasopressin (1 mu./ml. and 100 mu./ml.) in isolated toad urinary bladders (Bufo marinus) following overnight incubation in the presence or absence of steroid‐containing Ringer solution. 2. The water transport response to the lower dose of vasopressin (1 mu./ml.) was considerably reduced in 'steroid depleted' conditions, wheras the response to the higher dose of vasopressin (100 mu./ml.) was not similarly affected. 3. Aldosterone 3. Aldosterone 3. Aldosterone (10(‐7)M) potentiated the water transport response to the lower dose of vasopressin (1 mu./ml.) but had no effect on the response to the higher dose (100 mu./ml.). 4. There was no effect of 'steroid depletion' or aldosterone treatment on the vasopressin s.c.c. response when measured as a percentage increase above basal levels. 5. In 'steroid depleted' conditions vasopressin (1 mu./ml.) maximally stimulated Na+ transport (s.c.c.) but a higher dose of vasopressin (100 mu./ml.) was required for maximum water transport. 6. We have failed to obtain any potentiation effect of corticosterone (10(‐7)M) on the water transport or s.c.c. response to vasopressin (1 mu./ml.).

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Effects of Vasopressin on Toad Bladder Membrane Proteins: Relationship to Transport of Sodium and Water

Cited by 25 publications

References 7 publications

Membrane pathways for water and solutes in the toad bladder: I. Independent activation of water and urea transport

Membrane pathways for water and solutes in the toad bladder: I. Independent activation of water and urea transport

Membrane structural and functional responses to vasopressin in toad bladder

Effect of steroid depletion on the response of toad bladder to vasopressin.

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