Sodium compartmentation in turtle bladder

1963 ◽  
Vol 78 (4) ◽  
pp. 767-768 ◽  
Author(s):  
Clair M. Paine ◽  
E.C. Foulkes
Keyword(s):  
Turtle Bladder

Calcium transport in turtle bladder

1987 ◽  
Vol 253 (6) ◽  
pp. R917-R921
Author(s):  
S. Sabatini ◽  
N. A. Kurtzman
Keyword(s):  
Calcium Transport ◽  
Calcium Absorption ◽  
Short Circuit ◽  
Open Circuit ◽  
Calcium Flux ◽  
Bladder Epithelium ◽  
Control Value ◽  
Sodium Calcium ◽  
Turtle Bladder ◽  
Absorptive Flux

Unidirectional 45Ca fluxes were measured in the turtle bladder under open-circuit and short-circuit conditions. In the open-circuited state net calcium flux (JnetCa) was secretory (serosa to mucosa) and was 388.3 +/- 84.5 pmol.mg-1.h-1 (n = 20, P less than 0.001). Ouabain (5 X 10(-4) M) reversed JnetCa to an absorptive flux (serosal minus mucosal flux = -195.8 +/- 41.3 pmol.mg-1.h-1; n = 20, P less than 0.001). Amiloride (1 X 10(-5) M) reduced both fluxes such that JnetCa was not significantly different from zero. Removal of mucosal sodium caused net calcium absorption; removal of serosal sodium caused calcium secretion. When bladders were short circuited, JnetCa decreased to approximately one-third of control value but remained secretory (138.4 +/- 54.3 pmol.mg-1.h-1; n = 9, P less than 0.025). When ouabain was added under short-circuit conditions, JnetCa was similar in magnitude and direction to ouabain under open-circuited conditions (i.e., absorptive). Tissue 45Ca content was approximately equal to 30-fold lower when the isotope was placed in the mucosal bath, suggesting that the apical membrane is the resistance barrier to calcium transport. The results obtained in this study are best explained by postulating a Ca2+-ATPase on the serosa of the turtle bladder epithelium and a sodium-calcium antiporter on the mucosa. In this model, the energy for calcium movement would be supplied, in large part, by the Na+-K+-ATPase. By increasing cell sodium, ouabain would decrease the activity of the mucosal sodium-calcium exchanger (or reverse it), uncovering active calcium transport across the serosa.

BAFILOMYCIN A1 AT NANOMOLAR CONCENTRATIONS SATURABLY INHIBITS A PORTION OF TURTLE BLADDER ACIDIFICATION CURRENT

2001 ◽  
Vol 204 (16) ◽  
pp. 2911-2919
Author(s):  
STEVEN J. YOUMANS ◽  
CATHERINE R. BARRY
Keyword(s):  
Urinary Bladder ◽  
Acid Secretion ◽  
Dose Response ◽  
Response Curve ◽  
Collecting Duct ◽  
Dose Response Curve ◽  
Serosal Side ◽  
Bafilomycin A1 ◽  
Transport Activity ◽  
Turtle Bladder

SUMMARY An earlier report indicated that acid secretion in turtle urinary bladder is driven by an unusual vacuolar H+-ATPase and that the ATPase accounts for essentially all acid secreted. These results, however, are difficult to reconcile with the acid transporters currently ascribed to the renal collecting duct. Here, we re-examine the effect of bafilomycin A1, an inhibitor of vacuolar (V-type) H+-ATPases, on acid secretion by intact isolated bladders from Pseudemys scriptaturtles. Serosal-side bafilomycin had no effect on the transepithelial acidification current (AC). In the mucosal solution, bafilomycin inhibited the AC, with inhibition developing over the range 0.1-10 nmol l-1, with a sigmoidal dose—response curve, and an IC50 of 0.47 nmol l-1. At saturation, approximately 70 % of H+ secretion was inhibited. The remaining 30 % could be abolished by 30 μmol l-1 Sch-28080, which is a level that in other systems is known to inhibit H+/K+-ATPase transport activity specifically and essentially completely. When the order of addition was reversed (Sch-28080 first), there was no change in the magnitude of the effect produced by either inhibitor, and the two together again eliminated the AC. The data indicate that baseline acid secretion in intact bladders is due (i) in part to a highly bafilomycin-sensitive process, with sensitivity typical of vacuolar H+ ATPases; and (ii) in part to a more bafilomycin-resistant process that is sensitive to Sch-28080.

Glycogen in isolated mucosal and serosal fractions of turtle bladder

1971 ◽  
Vol 241 (2) ◽  
pp. 628-636 ◽  
Author(s):  
M.E. Lefevre ◽  
L.J. Dox ◽  
J.F. Gennaro ◽  
W.A. Brodsky
Keyword(s):  
Turtle Bladder

Role of membrane fusion in CO2 stimulation of proton secretion by turtle bladder

1983 ◽  
Vol 245 (1) ◽  
pp. C113-C120 ◽  
Author(s):  
D. L. Stetson ◽  
P. R. Steinmetz
Keyword(s):  
Deuterium Oxide ◽  
Cell Structure ◽  
Proton Secretion ◽  
Luminal Membrane ◽  
Turtle Bladder ◽  
Cytoplasmic Vesicles ◽  
Resultant Increase ◽  
Electron Lucent ◽  
Stimulation Of

The changes in cell structure produced during stimulation of proton secretion by CO2 in turtle bladder were examined using ultrastructural morphometric methods. One hour after CO2 addition, the area of the luminal membrane of the carbonic anhydrase-containing (CA) cell population was increased 2.5-fold and the volume percent of electron-lucent cytoplasmic vesicles in these CA cells was decreased by 61%. No changes were observed in the epithelial granular cells. These results suggest that during CO2 stimulation the vesicles fuse with the luminal membrane. CO2 stimulation of proton secretion is inhibited by the cytoskeleton-disrupting drugs colchicine and cytochalasin B and by 99% deuterium oxide as the Ringer solvent. Deuterium oxide also inhibits the decrease in cytoplasmic vesicles. Thus stimulation of proton secretion by turtle bladder CA cells depends to a large extent on vesicle fusion and the resultant increase in luminal surface area.

Evidence for proton transport by turtle bladder in presence of ambient bicarbonate

1970 ◽  
Vol 218 (3) ◽  
pp. 845-850 ◽  
Author(s):  
HH Green ◽  
PR Steinmetz ◽  
HS Frazier
Keyword(s):  
Proton Transport ◽  
Turtle Bladder

Aldosterone response in the turtle bladder is associated with an increase in ATP

1983 ◽  
Vol 245 (4) ◽  
pp. F512-F514
Author(s):  
N. Cortas ◽  
E. Abras ◽  
M. Walser
Keyword(s):  
Perchloric Acid ◽  
Sodium Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Open Circuit ◽  
Potential Difference ◽  
Freshwater Turtles ◽  
Active Sodium ◽  
Active Sodium Transport ◽  
Turtle Bladder

Urinary bladders from freshwater turtles, mounted as sacs, were stripped of their serosa and submucosa. This did not alter conductance. They were maintained in open circuit except for brief observation of short-circuit current (SCC) every 15 min. Potential difference (PD) averaged 68 +/- 14 mV and SCC 485 +/- 100 microA. Acetazolamide 10(-3) M increased SCC by 46 +/- 27 microA. Aldosterone 10(-7) M following acetazolamide resulted in a rise in SCC that began at about 75 min and reached a plateau between 3 and 5 h. SCC rose 127 +/- 15% compared with control bladder halves. ATP measured in perchloric acid extracts 5 h after addition of aldosterone increased by 33% (P less than 0.01) and (ATP)/(ADP) X (Pi) by 81% (P less than 0.01). These results support the view that the stimulatory effects of aldosterone on active sodium transport involve an increase in ATP and (ATP)/(ADP) X (Pi).

scholarly journals Exocytosis regulates urinary acidification in turtle bladder by rapid insertion of H+ pumps into the luminal membrane.

1982 ◽  
Vol 79 (14) ◽  
pp. 4327-4331 ◽  
Author(s):  
S. Gluck ◽  
C. Cannon ◽  
Q. Al-Awqati
Keyword(s):  
Luminal Membrane ◽  
Urinary Acidification ◽  
Turtle Bladder

Effect of parathyroid hormone on transport by toad and turtle bladder

1987 ◽  
Vol 252 (1) ◽  
pp. R63-R68
Author(s):  
S. Sabatini ◽  
N. A. Kurtzman
Keyword(s):  
Parathyroid Hormone ◽  
Epithelial Cells ◽  
Calcium Uptake ◽  
Short Circuit ◽  
Calcium Ionophore ◽  
Toad Bladder ◽  
Base Line ◽  
Ionophore A23187 ◽  
45Ca Uptake ◽  
Turtle Bladder

We recently demonstrated that parathyroid hormone (PTH) inhibited both vasopressin- and cyclic AMP-stimulated water transport in the toad bladder. This was associated with an increase in calcium uptake by isolated epithelial cells. We postulated that PTH exerts its action on H2O transport by directly stimulating calcium uptake. The current study was designed to compare the effects of PTH and the calcium ionophore, A23187, on H2O and Na transport and H+ secretion in toad and turtle bladders. In toad bladder, PTH and A23187 decreased arginine vasopressin (AVP)-stimulated H2O flow and short-circuit current (SCC) after 60 min serosal incubation. In turtle bladder A23187 decreased SCC to 79.3 +/- 3.6% of base line (P less than 0.05), and significantly decreased RSCC as well. PTH had no effect on SCC or H+ secretion in turtle bladders. Both PTH and A23187 increased 45Ca uptake in toad bladder epithelial cells; only A23187 increased 45Ca uptake in the turtle bladder. The different action of PTH in these two membranes, compared with that of the calcium ionophore, illustrates the selectivity of PTH on membrane transport. PTH increases calcium uptake and decreases transport only in a hormone-sensitive epithelium, whereas the ionophore works in virtually all living membranes. The mode of action of these two agents to increase calcium uptake is, therefore, likely different.

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