Sodium transport by isolated epithelium of the urinary bladder of the freshwater turtle

A B S T R A C T Addition of HCOi-to the serosal side (S) of the isolated turtle bladder results in a HCO0-flow from S to the mucosal side (M) which markedly reduces the net rate of acid secretion. To characterize the driving forces for this downhill HCO3-flow, the effects of metabolic inhibitors and substrates were examined. In short-circuited bladders with the M pH lowered to the point of zero net H+ secretion, the rate of HCO-entry into M in response to a 20-mM HCO3-gradient was measured by pH stat titration. Deoxygenation reduced the HC03-flux from 1.24±0.1 gM/h/8 cm2 (SEM) to 0.50±0.1 tM/h with glucose (2 X 10' M) and from 1.32±0.1 to 0.47±0.1 iAM/h without glucose.A similar reduction (61%) was observed in the presence of 1% C02. Dinitrophenol (10' M), cyanide (10' M), and deoxyglucose (10-' M) inhibited the HCO3-flux by 39%, 37%, and 38%, respectively. The combination of any of these inhibitors with N2 caused the same inhibition as Ns alone. In bladders depleted of substrate, pyruvate (5 X 10-' M) increased the HCOs-flux from 0.36 ±0.05 to 0.58±0.01 ,M/h (P < 0.005); the increment was abolished by deoxygenation.The results indicate that the bulk of the downhill HCOi-flow in this system is dependent on metabolic energy derived primarily from oxidative sources, and that this energy-dependent flow approximates the electroneutral component of HCO3-secretion that is coupled to Cl-absorption.

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“…Klahr and Bricker (11) and Nakagawa, Klahr, and Bricker (12) showed that Na+ transport is not abolished during deoxygenation and exposure to KCN.…”

Section: Discussionmentioning

confidence: 99%

Energy dependence of urinary bicarbonate secretion in turtle bladder.

Oliver¹,

Himmelstein²,

Steinmetz³

1975

J. Clin. Invest.

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“…The rate of Na transport which can be accurately assessed by the SCC [15], is influenced by the availability of substrate and oxygen, and mucosal Na concentration. When Na transport is totally inhibited by ouabain the SCC reverses and the mucosa becomes positive in relation to the serosa [19].…”

Section: Discussionmentioning

confidence: 99%

“…The bladder of the fresh water turtle and that of the toad are capable of transporting Na and secreting H + in vitro [1,2,15,[18][19][20][21][22]24]. The toad bladder is also capable of water transport in response to vasopressin [4,7,9].…”

Section: * Mailing Address and To Whom Reprint Request Should Be Madementioning

confidence: 99%

“…These experiments were performed on the stripped mucosa of the turtle bladder utilizing the method of Nagakawa et al [15] to separate the mucosa from the remaining tissues. For the calcium uptake experiments, all hemibladders were preincubated in 10 ml of oxygenated turtle Ringer's solution containing 5 x 10-4 M ouabain for 10 rain.…”

Section: Radioactive Calcium Uptake and Calcium Effluxmentioning

confidence: 99%

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Effect of quinidine on Na, H+, and water transport by the turtle and toad bladders

Arruda¹,

Sabatini²

1980

J. Membrain Biol.

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The effect of quinidine on Na and H+ transport by the turtle bladder and water transport by the toad bladder was examined. Quinidine inhibited the short-circuit current and the potential difference in a dose-dependent fashion. The effect of quinidine on the short-circuit was not dependent on extracellular calcium concentration and was not reversible with removal of the drug. Quinidine inhibited H+ secretion in a dose-dependent fashion. The effect of quinidine on H+ secretion also was not dependent on extracellular calcium concentration and was not reversible, either with removal of the drug or with stimulation of H+ secretion with 5% CO2. The effect of quinidine on Na or H+ transport could not be elicited by an equivalent dose of tetracaine, suggesting that the inhibitory effect of quinidine is not dependent on its anesthetic properties. Quinidine also inhibited vasopressin and cyclic AMP stimulated water flow in the toad bladder. Quinidine did not alter calcium uptake by the turtle bladder but increased calcium efflux by the turtle and toad bladders. These observations suggest that a rise in cytosolic calcium is responsible for the inhibitory effect of quinidine on Na, H+, and water transport.

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“…For this, bladders were dissected into mucosal and serosal fractions as described previously [19,20,24] and the two fractions utilized separately. The major components of the bladder wall and their proportions have been defined [19].…”

Section: Methodsmentioning

confidence: 99%

Metabolism of depleted turtle bladder

1972

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Summary. Oxygen consumption, glycogen content, transmural potential difference (PD), and short-circuit current (SCC) were measured in fresh turtle hemibladder sacs and in matching sacs depleted by 18 hr of incubation in aerated, substrate-free Ringer's solution. Percent of original values after depletion were: oxygen consumption, 61%; glycogen content, 36%; PD, 28%; SCC, 19%. PD and SCC responded to addition of substrate (5.5 mM glucose plus 2 mu pyruvate) by a lag period of approximately 2 hr followed by progressive increases lasting for many hours. Other experiments utilized split bladders. The epithelium and adhering connective tissue (mucosal fraction) were separated from the underlying smooth muscle and connective tissue (serosal fraction) and the oxygen consumption and glycogen content of slices of the two fractions determined. Mucosal oxygen consumption declined to 48 % of the original value during depletion while serosal oxygen consumption (initially much lower than mucosal) was well-maintained at 95 % of the original value. Substantial net synthesis of glycogen took place in both fractions of depleted bladders after addition of substrate. The ratio of moles of oxygen consumed to moles of glucose (from glycogen) disappearing during the 18-hr depletion period was approximately 5.5 for serosal tissue and within the range 30 to 61 for mucosal tissue. The mucosal ratio was incompatible with the utilization of glycogen as the major endogenous substrate during depletion under aerobic conditions. It is suggested that the oxidation of lipid supports most of the endogenous metabolism in the mucosal tissue of the turtle bladder.Tissues depleted of endogenous hormones and substrates by long incubation in minimal media have been found to be useful in characterizing transport processes [6,28,29]. Such tissues are assumed to use up or lose endogenous reserves and to become sensitive to the effects of added hormones or substrates. The isolated urinary bladder of the water turtle, a tissue known to carry on vigorous ion transport [9,10,15,31], shows good viability under depletion conditions [17]. To evaluate changes taking place in turtle bladders during depletion, glycogen levels, respiration rates, short-circuit

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Sodium transport by isolated epithelium of the urinary bladder of the freshwater turtle

Cited by 18 publications

References 0 publications

Energy dependence of urinary bicarbonate secretion in turtle bladder.

Energy dependence of urinary bicarbonate secretion in turtle bladder.

Effect of quinidine on Na, H+, and water transport by the turtle and toad bladders

Metabolism of depleted turtle bladder

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