Effect of vasopressin on toad bladder under conditions of zero net sodium transport

Civan, MM; Kedem, O.; Leaf, Alexander

doi:10.1152/ajplegacy.1966.211.3.569

Cited by 66 publications

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“…one that is not directly coupled to the supply of metabolic energy through an ouabain-sensitive ATPase. Therefore the effect ofADH on JOT observed in these experiments supports the assumption that ADH acts primarily on a passive mechanism (Civan, Kedem & Leaf, 1966). Fig.…”

Section: Discussionsupporting

confidence: 84%

The effect of antidiuretic hormone on Na movement across frog skin

Cereijido¹,

Rotunno²

1971

The Journal of Physiology

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SUMMARY1. The effect of antidiuretic hormone (ADH) on the movement and distribution of Na was studied. This was done using three different approaches: (a) the measurement of Na and 22Na in slices of epithelium of skins which were exposed to Ringer of varied composition containing 22Na, (b) the measurement of the influx of Na from the outer to the inner bathing solution with 22Na added to the outside, and (c) the use of a recently introduced technique which permits the direct evaluation of the flux from the outer solution -÷ epithelium, (JOT), i.e. the flux across the barrier which is generally regarded as the site of ADH activity.2. ADH increased the influx from the outer to the inner bathing solution of Na (50 %) not only when the concentration of Na on the outside was 115 mM (i.e. higher than in the epithelium) but even when the concentration was 1 mM (67 %).3. When the skin was bathed with 1mM-Na Ringer on the outside, ADH increased the unidirectional Na flux JOT by 56 % (Rana pipiens) and 71 % (Leptodactylus ocellatus). When the concentration was 115 mm a small increase (17 %) was observed in paired skins of R. pipiens. Under this condition no change was observed in L. ocellatus. 4. The amount of epithelial sodium which is labelled by 22Na added to the outside was taken to reflect the amount of Na involved in Na transport across the epithelium. Depending on whether the concentration of Na on the outside was high (115 mM) or low (1 mM), ADH produced an increase, or a decrease, of both the total Na content and the amount of 22Na exchanged.5. When the concentration of Na on the outside was low, ADH increased the total influx and JOT in spite of the fact that it lowers the total Na content and does not affect the exchangeable pool of Na. This observation is inconsistent with the view that the effect of ADH is due to the fact M. CEREIJIDO AND C. A. ROTUNNO that the increased permeability of the outer barrier allows more Na into the cell, and that the resulting increase of Na concentration in the cytoplasm accelerates the Na pumps at the inner side of the cells.6. It is concluded that ADH speeds up Na movements at the outward facing barrier, and that this exchange which facilitates the penetration of Na into a transporting compartment produces also a gain or a loss of Na in compartments not directly involved in Na transport across the epithelium. One compartment which is not involved in Na transport might be the cytoplasm of the epithelial cells.

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Section: Discussionsupporting

confidence: 84%

The effect of antidiuretic hormone on Na movement across frog skin

Cereijido¹,

Rotunno²

1971

The Journal of Physiology

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“…Interest in the value of ENa is based on the perception that it represents a fundamental characteristic of the sodium transport system. Its numerical value has been estimated under a large variety of experimental conditions, and a broad range of values from some 80 mV to 240 mV has been reported (7,(14)(15)(16). Changes in the apparent "ENa" with changes in transepithelial electrochemical potential have been observed by other investigators (16,17).…”

Section: Relationship Of "Ena" To Aip and Jnamentioning

confidence: 82%

Energetics of sodium transport in toad urinary bladder.

Canessa¹,

Labarca²,

DiBona³

et al. 1978

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

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The ratio of the rate of transepithelial sodium trans ort, JNa, across the isolated toad urinary bladder to the simultaneously measured rate of transport-dependent metab- Previous studies from this laboratory (1) have examined the coupling of active sodium transport to metabolism in the isolated urinary bladder of the toad Bufo marinus. The urinary bladder of the toad reabsorbs sodium salts from the bladder urine and can do so against large gradients of sodium concentration-i.e., 1.0 meq/liter in urine to 120 meq/liter in toad serum-and against electrical potentials of 10 to 100 mV serosal surface positive to urine (2). This is accomplished by the single layer of epithelial cells lining the bladder wall, which draw sodium ions from the urine into the cells and then actively pump the sodium from the cell out through the basolateral plasma membranes into the serosal medium or the body fluids of the toad. The anion follows the sodium passively, moving apparently through paracellular pathways between the epithelial cells. We found that the ratio of sodium transported across the isolated bladder to the suprabasal-i.e., transport related-CO2 production remains constant despite imposing hyperpolarizing or depolarizing electrical potentials across the tissue. Applying a hyperpolarizing voltage clamp across the bladder increases the work the tissue must do for each sodium ion reabsorbed, while depolarizing the tissue reduces the work necessary to transport sodium. Thus one might have expected that the metabolic cost of "uphill" sodium transport would exceed that for "downhill" transport, in which case the depolarizing transepithelial potential assists in driving sodium from urine to serosal medium through the transport pathway.In the present study the relation of sodium transport to metabolism has been redetermined over the physiologic range of transepithelial potentials from 0 to +90 mV hyperpolarizing potentials. In addition to confirming that the stoichiometry of sodium transport to metabolism remains constant, this study allows an evaluation of the driving force of the sodium transportThe publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U. S. C. §1734 solely to indicate this fact. 4591process. It was observed that the driving force for sodium transport increased with increasing hyperpolarization of the bladder and with the associated decrease in active sodium transport; the latter is the relevant variable accounting for the changes in the estimated driving force.MATERIALS AND METHODS Urinary hemibladders from female toads, Bufo marinus, were used. The techniques and equipment employed were as previously described (1, 3). Special care was taken to avoid tissue damage or crushing at the margins of the mounted bladders, and only bladders with spontaneous transepithelial potentials, A4f, of +70 mV or greater and with passive conductance less than 50% of the total transepithelial conductance at +50 mV ...

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“…The hydroxyl ions remaining are disposed of with the aid of cytoplasmic carbonic anhydrase by combining with C02; the HC0-so formed then diffuses down an electrochemical gradient into the serosal side. By analogy with the sodium transport system (8,11) this process can be represented by an equivalent circuit made up of a battery representing the proton pump, a resistance in series with the pump and a shunt resistance in parallel with the pump. The force of the pump, the PMF, can be evaluated following Ussing and Zerahn (8), as the transepithelial gradient necessary to bring net transport to zero.…”

Section: Discussionmentioning

confidence: 99%

Characteristics of stimulation of H+ transport by aldosterone in turtle urinary bladder.

Al‐Awqati¹,

Norby²,

Mueller³

et al. 1976

J. Clin. Invest.

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A B S T R A C T Aldosterone stimulates not only Na4 absorption but also urinary acidification. In this investigation the effects of aldosterone on H4 transport are examined in vitro in turtle bladder, a urinary membrane in which several of the factors controlling H4 transport have been defined. H+ transport was increased in bladder halves exposed to aldosterone compared to control halves. Stimulation of H4 secretion was observed as early as 1 h after addition of aldosterone and occurred before that of Na4 transport. In bladders depleted of endogenous substrate addition of glucose increased H+ transport more in aldosterone-treated halves (10.0±1.3 nmol/min) than in control halves (6.8±2.3). Addition of pyruvate failed to increase H+ transport (-0.3+0.7) in control halves but caused significant increments (2.4±0.5) in aldosterone-treated halves. In aldosteronetreated bladders glucose caused larger increments (16.5 ±2.7) in H+ transport than pyruvate (9.3±2.0) when halves of the same bladders were compared. Na+ transport, however, was equally increased by the two substrates. Despite the differences in time course and substrate requirements between the stimulation of H+ and Na+ transport, both increases were abolished by actinomycin-D.To examine the effect of aldosterone on the force of the H+ pump, protonmotive force, the pH gradient that would nullify the transport rate was determined with and without aldosterone. Aldosterone did not alter protonmotive force but significantly increased the slope of the H+ transport rate on the applied pH gradient. It is concluded that aldosterone stimulates H4 transport independently of Na+ transport. It increases the responsiveness of the transport rate to glucose and to a lesser extent pyruvate, an effect probably secondary to the increased transport rate. Equivalent circuit analysis indicates that aldosterone facilitates the flow of protons through the active transport pathway but does not increase the force of the pump. INTRODUCTION Several lines of evidence indicate that aldosterone not only stimulates the renal absorption of sodium but also the process of urinary acidification. To which extent the increased acidification is a function of accelerated sodium absorption remains to be determined. At least some studies suggest that acidification may be stimulated independently of sodium transport. Lifschitz et al.(1) provided some evidence in the dog that renal H4 secretion is stimulated by a pathway that does not involve DNA-dependent synthesis of RNA. Ludens and Fanestil (2) reported that aldosterone increased the rate of acidification in the urinary bladder of the Colombian toad, as judged from the reversed short-circuit current after inhibition of sodium transport; they did not attempt, however, to explore the transport step in acidification that was stimulated by the hormone.Since turtle urinary bladder responds to aldosterone (3) and is capable of urinary acidification under conditions that permit close examination of the transport components (4), this preparation was se...

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Effect of vasopressin on toad bladder under conditions of zero net sodium transport

Cited by 66 publications

References 0 publications

The effect of antidiuretic hormone on Na movement across frog skin

The effect of antidiuretic hormone on Na movement across frog skin

Energetics of sodium transport in toad urinary bladder.

Characteristics of stimulation of H+ transport by aldosterone in turtle urinary bladder.

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