Active transport of calcium across the urinary bladder and colon of the toad Bufo marinus

1983 ◽  
Vol 245 (1) ◽  
pp. R91-R94 ◽  
Author(s):  
C. J. Rosoff ◽  
G. F. Baldwin ◽  
P. J. Bentley

Unidirectional fluxes of calcium were measured (in vitro) across the urinary bladder and colon of the toad Bufo marinus in the absence of electrochemical gradients. A net calcium flux was observed in each tissue, but the polarity differed; it occurred from the mucosal (luminal) to the serosal side of the colon and from the serosal to mucosal (urinary) side of the bladder. The active transport in each tissue appeared to involve different mechanisms; that across the colon exhibited a sodium dependence, possibly involving a sodium-calcium exchange, but this was not seen in the urinary bladder. The net flux in the latter was, however, abolished by metabolic inhibitors, possibly reflecting a role of a calcium-adenosine triphosphatase mechanism. The results are discussed in relation to the calcium metabolism of this amphibian.

1958 ◽  
Vol 17 (3) ◽  
pp. 201-209 ◽  
Author(s):  
P. J. BENTLEY

SUMMARY 1. An in vitro preparation of the urinary bladder of Bufo marinus is described. 2. Small doses of 'Pituitrin' markedly increase the rate of water transfer across the bladder wall when the solutions inside the bladder are hypotonic. 3. Passive movement is small and increases slightly with increases in the osmotic gradient across the bladder wall. It is unaffected by changes in substrate levels or any of the metabolic inhibitors tested except for cyanide which increases it in some cases. 4. The vasopressor neurohypophysial fraction is more active than the oxytocic one in increasing water transfer across the bladder wall. 5. The increase in water transfer depends on an intact oxygen supply and sufficient glucose or pyruvate. 6. Iodoacetate, malonate, cyanide, 2–4-dinitrophenol, and bubbling 5% CO2+95% O2 through Ringer's solution inhibit the water transfer in response to neurohypophysial extract. 7. Diamox is only an effective inhibitor at very high concentrations. 8. The possible mechanism of the water transfer is discussed.


1959 ◽  
Vol 18 (4) ◽  
pp. 327-333 ◽  
Author(s):  
P. J. BENTLEY

SUMMARY 1. The effects of ionic changes in the bath fluids on water transfer across an in vitro preparation of the urinary bladder of the toad Bufo marinus were investigated. 2. Calcium was necessary to maintain the normal low permeability of the bladder to water in the absence of Pituitrin. Magnesium, strontium and manganese but not barium could substitute for calcium. 3. With low concentration of calcium there was a reduction in the water transfer across the bladder wall in response to Pituitrin and no other divalent ion could substitute for calcium. 4. Exclusion of potassium from the serosal side of the bladder reduced the water transfer in the presence of Pituitrin. Increase in potassium concentration above normal levels also inhibited the response to hormone. When no Pituitrin was present there was no change in water loss from the bladder with alterations in potassium concentration. Absence of potassium from the epithelial side of the bladder had no effect whether Pituitrin was present or not. 5. The presence of sodium on the epithelial side increased the water transfer in response to Pituitrin and neither lithium, choline nor potassium could substitute for it. Replacement of 50% of the sodium chloride on the serosal side of the bladder by choline chloride decreased the water transfer in response to Pituitrin.


1968 ◽  
Vol 26 (1) ◽  
pp. 57-68 ◽  
Author(s):  
Stewart A Middler ◽  
Charles R Kleeman ◽  
Eleanor Edwards

1992 ◽  
Vol 262 (3) ◽  
pp. F442-F448 ◽  
Author(s):  
N. S. Krieger ◽  
N. E. Sessler ◽  
D. A. Bushinsky

Metabolic acidosis induces net calcium flux (JCa) from cultured neonatal mouse calvariae through physicochemical and cell-mediated mechanisms. To determine the role of osteoblasts in acid-induced JCa, collagen synthesis and alkaline phosphatase activity were assessed in calvariae incubated in reduced pH and bicarbonate medium, a model of metabolic acidosis (Met), and compared with controls (Ctl). Collagen synthesis fell from 30.5 +/- 1.1 in Ctl to 25.1 +/- 0.4% with Met, and alkaline phosphatase decreased from 403 +/- 25 in Ctl to 298 +/- 21 nmol Pi.min-1.mg protein-1 with Met. During acidosis JCa was correlated inversely with percent collagen synthesis (r = -0.743, n = 11, P = 0.009) and with alkaline phosphatase activity (r = -0.453, n = 22, P = 0.034). To determine the role of osteoclasts in acid-induced JCa, osteoclastic beta-glucuronidase activity was determined in Ctl and Met in the absence or presence of the osteoclastic inhibitor calcitonin (CT, 3 x 10(-9) M). Met increased beta-glucuronidase (5.9 +/- 0.2) compared with Ctl (4.6 +/- 0.3 micrograms phenolphthalein released.bone-1.h-1), whereas CT inhibited beta-glucuronidase in both Ctl and Met (3.1 +/- 0.2 and 3.5 +/- 0.3, respectively). During acidosis JCa was correlated directly with beta-glucuronidase activity (r = 0.683, n = 42, P less than 0.001). Thus the cell-mediated component of JCa during acidosis in vitro appears to result from a combination of inhibited osteoblastic and stimulated osteoclastic activity.


1986 ◽  
Vol 251 (2) ◽  
pp. G237-G242 ◽  
Author(s):  
J. E. Heubi

The role of thyroid hormone on the postnatal development of ileal active taurocholate transport uptake was measured by an in vitro incubation technique in Sprague-Dawley rats. In 16-day-old rats treated with pharmacological doses of L-thyroxine (50 micrograms X 100 g body wt-1 X day-1 on days 10-13), ileal active transport appeared precociously whose Km was 1.60 +/- 0.48 mM and Vapp (apparent maximal velocity) was 8.09 +/- 1.14 nmol X min-1 X mg dry wt-1, while age-matched shams had only passive diffusion of taurocholate. To determine whether enhanced endogenous secretion of thyroxine was capable of stimulating development of ileal active taurocholate transport, thyrotrophic stimulating hormone (TSH) (0.5 U/100 g body wt twice daily) was given on days 10-13, with uptake measured on day 16. Following TSH treatment, only passive transport for taurocholate was observed in the ileum; uptake rates were consistently higher than those for untreated controls at each study concentration. Thyroidectomy performed at age 14 days with uptake measured at age 21 days did not ablate development of ileal active transport but resulted in a significant reduction (P less than 0.001) in the Vapp (7.39 +/- 1.10 nmol X min-1 X mg dry wt-1) and a significant increase (P less than 0.014) in Km (1.72 +/- 0.53 mM) compared with age-matched controls. Thyroid hormone does not appear to be obligatory for the postnatal development of ileal active taurocholate transport.


1981 ◽  
Vol 240 (5) ◽  
pp. E550-E555
Author(s):  
S. Handwerger ◽  
P. M. Conn ◽  
J. Barrett ◽  
S. Barry ◽  
A. Golander

To study the effects of calcium on the release of human placental lactogen (hPL), placental explants were exposed to media containing lower or higher concentrations of calcium than normally available to the placenta. Explants exposed for 2 h to calcium-poor medium or medium containing either 2 mM EDTA or 2 mM EGTA released 160, 248, and 253% more hPL, respectively, than control explants. In contrast, explants exposed to medium containing higher than normal calcium concentrations released the same amounts of hPL as the control explants. At lower than normal extracellular calcium concentrations, the increased hPL release was inversely proportional to the calcium concentration. The increased release in calcium-poor medium was inhibited by subsequent exposure of the explants to medium containing calcium and was prevented by either barium or magnesium. Changes in barium or magnesium concentrations, however, had no effects on hPL release in the presence of normal extracellular calcium concentrations. Methoxyverapamil (D 600), an inhibitor of calcium flux, stimulated hPL release. Because low extracellular calcium and methoxyverapamil both inhibit calcium influx, these experiments suggest that calcium influx inhibits hPL release. The role of calcium in the regulation of hPL release therefore appears to be different from that reported in other release systems.


In several species of anurans, the in vivo skin has been shown to absorb Na + and Cl - independently from dilute external solutions. That the mechanism for sodium absorption is different from that of chloride absroption is born out by the following: (1) Either of these ions is absorbed without an accompanying ion when this latter is impermeant. (2) From NaCl solutions there can be an unequal absorption of sodium and chloride. (3) A selective inhibition of the absorption of one of the ions can be produced experimentally, while the net flux of the other remains unchanged. In all these situations, the absorbed ion has to be exchanged against an endogenous ion of the same charge. In Calyptocephalella gayi , H + and HCO - 3 are exchanged against sodium and chloride respectively. A comparison of the relationships between H + excretion and Na + absorption in vivo skins and shortcircuited in vitro skins shows that in the latter no H + excretion occurs, only the Na + transport being maintained under these experimental conditions. From this, one must conclude that the active Na + transport is the motive factor of the transport mechanism. H + excretion by the in vivo skin plays the role of physiologically short-circuiting the Na + transport.


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