THE SWELLING OF FROG BLADDER CELLS PRODUCED BY OXYTOCIN

1965 ◽  
Vol 33 (2) ◽  
pp. 171-177 ◽  
Author(s):  
J. V. NATOCHIN ◽  
K. JANÁČEK ◽  
R. RYBOVÁ
Keyword(s):  
Urinary Bladder ◽  
Water Flow ◽  
Osmotic Gradient ◽  
Frog Urinary Bladder ◽  
Intracellular Space ◽  
Osmotic Water ◽  
Inulin Space ◽  
Bladder Cells ◽  
Synthetic Oxytocin ◽  
Osmotic Water Flow

SUMMARY (1) Synthetic oxytocin (100 m-u./ml.) produces swelling of the isolated frog urinary bladder even in the absence of an osmotic gradient across the bladder. (2) Calculations show that the change in intracellular space does not necessarily differ significantly from that in the presence of an osmotic gradient since the inulin space is markedly affected by the osmotic water flow. (3) Part of the cellular potassium is exchanged for sodium during the swelling produced by oxytocin. (4) A possible mechanism and the significance of the swelling is discussed.

Polyclonal antibodies in study of ADH-induced water channels in frog urinary bladder

1991 ◽  
Vol 261 (3) ◽  
pp. F437-F442
Author(s):  
G. Valenti ◽  
G. Calamita ◽  
M. Svelto
Keyword(s):  
Urinary Bladder ◽  
Water Flow ◽  
Apical Membrane ◽  
Polyclonal Antibodies ◽  
Immune Serum ◽  
Frog Urinary Bladder ◽  
Hormonal Stimulation ◽  
Osmotic Water ◽  
Triton X ◽  
Osmotic Water Flow

It is now generally accepted that changes in water permeability in anti-diuretic hormone (ADH)-responsive target epithelial cells result from the insertion in the plasma apical membrane of new components that contain channels for water. The specificity of these channels suggests that they are formed by intrinsic proteins having access to both facies and spanning the whole membrane. We have previously shown that Triton X-100 apical extracts from ADH-stimulated frog urinary bladder contain some proteins inserted under hormonal stimulation. In the present study we have developed polyclonal antibodies using Triton X-100 extract as an immunogen. After considering the inhibitory effect exerted by the whole immune serum on the osmotic water flow, we used different adsorption steps to select, from the immune serum, antibodies to apical membrane proteins inserted in response to the hormone. Immunoblot analysis of these selected antibodies shows that they recognize seven to eight proteins, of which 55-, 35-, 26-, and 17-kDa proteins are always present. Antibodies to these four proteins, affinity purified on nitrocellulose sheets, inhibited ADH-induced osmotic water flow. Altogether these results strongly suggest that proteins of 55, 35, 26, and 17 kDa (or at least one of them) are likely to be involved in the mechanism of water transport.

Evidence for transcellular osmotic water flow in rat proximal tubules

1985 ◽  
Vol 249 (1) ◽  
pp. F124-F131 ◽  
Author(s):  
P. A. Preisig ◽  
C. A. Berry
Keyword(s):  
Surface Area ◽  
Water Flow ◽  
Water Permeability ◽  
Channel Length ◽  
Osmotic Gradient ◽  
Osmotic Water Permeability ◽  
Osmotic Water ◽  
Major Route ◽  
Osmotic Water Flow

To determine the predominant pathway for transepithelial osmotic water flow, the transepithelial osmotic water permeability [Pf(TE)] and the apparent dimensions of paracellular pores and slits were determined in rat proximal convoluted tubules microperfused in vivo. To measure Pf(TE), tubules were perfused with a hyposmotic, cyanide-containing solution. Pf(TE), calculated from the observed volume flux in response to the measured log mean osmotic gradient, was 0.12-0.15 cm/s, assuming sigmaNaCl equal to 1.0-0.7, respectively. The dimensions of the paracellular pathways were determined using measured sucrose and mannitol permeabilities (nonelectrolytes confined to the extracellular space). These were 0.43 and 0.87 X 10(-5) cm/s, respectively. By using the ratio of these permeabilities, their respective free solution diffusion coefficients and molecular radii, and the Renkin equation, the radius of the nonelectrolyte-permeable pores and the total pore area/cm2 surface area/channel length were calculated to be 1.4 nm and 3.56 cm-1, respectively. Similar calculations for slits yielded a slit half-width of 0.8 nm and a total slit area/cm2 surface area/channel length of 3.16 cm-1. The osmotic water permeability of these nonelectrolyte-permeable pathways was calculated by Poiseuille's law to be 0.0018 cm/s (pores) or 0.0014 cm/s (slits), at most 2% of Pf(TE). We conclude that the nonelectrolyte-permeable pathway in the tight junctions is not the major route of transepithelial osmotic water flow in the rat proximal tubule.

scholarly journals THE EFFECT OF SMOOTH MUSCLE ON THE INTERCELLULAR SPACES IN TOAD URINARY BLADDER

1970 ◽  
Vol 46 (2) ◽  
pp. 235-244 ◽  
Author(s):  
Donald R. DiBona ◽  
Mortimer M. Civan
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Water Flow ◽  
Toad Urinary Bladder ◽  
Reliable Index ◽  
Intercellular Spaces ◽  
Phase Microscopy ◽  
Osmotic Water ◽  
Smooth Muscle Relaxant ◽  
Osmotic Water Flow

Phase microscopy of toad urinary bladder has demonstrated that vasopressin can cause an enlargement of the epithelial intercellular spaces under conditions of no net transfer of water or sodium. The suggestion that this phenomenon is linked to the hormone's action as a smooth muscle relaxant has been tested and verified with the use of other agents effecting smooth muscle: atropine and adenine compounds (relaxants), K+ and acetylcholine (contractants). Furthermore, it was possible to reduce the size and number of intercellular spaces, relative to a control, while increasing the rate of osmotic water flow. A method for quantifying these results has been developed and shows that they are, indeed, significant. It is concluded, therefore, that the configuration of intercellular spaces is not a reliable index of water flow across this epithelium and that such a morphologic-physiologic relationship is tenuous in any epithelium supported by a submucosa rich in smooth muscle.

Blockade of colchicine-induced inhibition of vasopressin-stimulated osmotic water flow: failure to influence microtubule formation

1985 ◽  
Vol 249 (4) ◽  
pp. F464-F469
Author(s):  
D. A. Baron ◽  
R. M. Burch ◽  
P. V. Halushka ◽  
S. S. Spicer
Keyword(s):  
Urinary Bladder ◽  
Water Flow ◽  
Volume Fraction ◽  
Cyclooxygenase Inhibitors ◽  
Maximal Response ◽  
Prostaglandin E ◽  
Toad Urinary Bladder ◽  
Meclofenamic Acid ◽  
Osmotic Water ◽  
Osmotic Water Flow

Colchicine inhibits vasopressin-induced osmotic water flow across isolated toad urinary bladder. Concomitantly, colchicine has been shown to reduce the relative cytoplasmic volume fraction of microtubules in the apical granular cells of this epithelium that have been shown previously to mediate the hydroosmotic effect of vasopressin. Therefore, an intact cytoskeleton has been postulated to be a requirement for a full response to vasopressin. Since it has been demonstrated recently that cyclooxygenase inhibitors (meclofenamic acid) abrogate the inhibition by colchicine of vasopressin-stimulated water flow, we tested by stereological criteria the hypothesis that colchicine in the presence of meclofenamic acid does not prevent the polymerization of tubulin. Our results show that the relative cytoplasmic volume fraction of microtubules was reduced 75% by colchicine in the presence or absence of meclofenamic acid. An alternative explanation of the inhibitory action of colchicine is its ability in the toad urinary bladder to enhance the endogenous synthesis of and sensitivity to prostaglandin E, a potent negative modulator of vasopressin-stimulated water flow. An intact microtubular component of the cytoskeleton does not appear to be required for a maximal response to a physiological dose of vasopressin.

Effect of colchicine on the osmotic water flow across the toad urinary bladder

1975 ◽  
Vol 413 (2) ◽  
pp. 277-282 ◽  
Author(s):  
Shigekazu Yuasa ◽  
Shigeharu Urakabe ◽  
Genjiro Kimura ◽  
Dairoku Shirai ◽  
Yoshihiro Takamitsu ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Water Flow ◽  
Toad Urinary Bladder ◽  
Osmotic Water ◽  
Osmotic Water Flow

Effects of prostacyclin on short-circuit current and water flow in the toad urinary bladder

1983 ◽  
Vol 244 (3) ◽  
pp. F270-F277
Author(s):  
T. Pohlman ◽  
J. Yates ◽  
P. Needleman ◽  
S. Klahr
Keyword(s):  
Urinary Bladder ◽  
Water Transport ◽  
Water Flow ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Toad Bladder ◽  
Camp Production ◽  
Acid Product ◽  
Osmotic Water ◽  
Osmotic Water Flow

The effects of prostaglandins of the E series on sodium and water transport have been studied extensively. PGE2 has been shown to inhibit the increase in osmotic water flow produced by vasopressin and to stimulate short-circuit current (SCC) in the toad bladder. On the other hand, the effects of prostacyclin (PGI2), an arachidonic acid product, on sodium and water transport have not been extensively evaluated. The present studies describe the effects of PGI2 on basal and vasopressin-stimulated osmotic water flow and on SCC in the urinary bladder of the toad. Studies were performed in the absence or presence of indomethacin. PGI2 in the absence of indomethacin had no effect on basal or vasopressin-stimulated osmotic water flow. When indomethacin was present, thereby eliminating intrinsic prostaglandin biosynthesis, PGI2 inhibited basal but not vasopressin-stimulated osmotic water flow. PGI2 increased SCC in the presence or absence of indomethacin. 6-keto PGF1 alpha, the stable metabolite of PGI2, had no effect on SCC. PGI2 stimulated cAMP production in isolated toad bladder epithelial cells. 2',5'-Dideoxyadenosine, an inhibitor of cAMP production, blocked the increase in SCC produced by PGI2, suggesting that the effects of this compound on SCC are mediated via cAMP.

scholarly journals A model of electrodiffusion and osmotic water flow and its energetic structure

2011 ◽  
Vol 240 (22) ◽  
pp. 1835-1852 ◽  
Author(s):  
Yoichiro Mori ◽  
Chun Liu ◽  
Robert S. Eisenberg
Keyword(s):  
Water Flow ◽  
Osmotic Water ◽  
Osmotic Water Flow
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