Suppression of fatty acid β-oxidation and energy deficiency as a cause of inhibitory effect of E. coli lipopolysaccharide on osmotic water transport in the frog urinary bladder

2019 ◽  
Vol 218 ◽  
pp. 81-87
Author(s):  
Ekaterina Fock ◽  
Elena Lavrova ◽  
Vera Bachteeva ◽  
Svetlana Nikolaeva ◽  
Rimma Parnova
Keyword(s):  
Fatty Acid ◽  
Urinary Bladder ◽  
Water Transport ◽  
Inhibitory Effect ◽  
Frog Urinary Bladder ◽  
Energy Deficiency ◽  
E Coli ◽  
Osmotic Water

Prostaglandin E2 inhibits vasotocin-induced osmotic water permeability in the frog urinary bladder by EP1-receptor-mediated activation of NO/cGMP pathway

2007 ◽  
Vol 293 (1) ◽  
pp. R528-R537 ◽  
Author(s):  
Vera Bachteeva ◽  
Ekaterina Fock ◽  
Elena Lavrova ◽  
Svetlana Nikolaeva ◽  
Stepan Gambaryan ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Urinary Bladder ◽  
Water Permeability ◽  
Inhibitory Effect ◽  
No Synthase ◽  
Arginine Vasotocin ◽  
Osmotic Water Permeability ◽  
Frog Urinary Bladder ◽  
Osmotic Water ◽  
Cgmp Pathway

PGE2 is a well-known inhibitor of the antidiuretic hormone-induced increase of osmotic water permeability (OWP) in different osmoregulatory epithelia; however, the mechanisms underlying this effect of PGE2 are not completely understood. Here, we report that, in the frog Rana temporaria urinary bladder, EP1-receptor-mediated inhibition of arginine-vasotocin (AVT)-induced OWP by PGE2 is attributed to increased generation of nitric oxide (NO) in epithelial cells. It was shown that the inhibitory effect of 17-phenyl-trinor-PGE2 (17-ph-PGE2), an EP1 agonist, on AVT-induced OWP was significantly reduced in the presence of 7-nitroindazole (7-NI), a neuronal NO synthase (nNOS) inhibitor. NO synthase (NOS) activity in both lysed and intact epithelial cells measured as a rate of conversion of l-[3H]arginine to l-[3H]citrulline was Ca2+ dependent and inhibited by 7-NI. PGE2 and 17-ph-PGE2, but not M&B-28767 (EP3 agonist) or butaprost (EP2 agonist), stimulated NOS activity in epithelial cells. The above effect of PGE2 was abolished in the presence of SC-19220, an EP1 antagonist. 7-NI reduced the stimulatory effect of 17-ph-PGE2 on NOS activity. 17-ph-PGE2 increased intracellular Ca2+ concentration and cGMP in epithelial cells. Western blot analysis revealed an nNOS expression in epithelial cells. These results show that the inhibitory effect of PGE2 on AVT-induced OWP in the frog urinary bladder is based at least partly on EP1-receptor-mediated activation of the NO/cGMP pathway, suggesting a novel cross talk between AVT, PGE2, and nNOS that may be important in the regulation of water transport.

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.

AVP-independent high osmotic water permeability of frog urinary bladder and autacoids

1996 ◽  
Vol 433 (1-2) ◽  
pp. 136-145 ◽  
Author(s):  
Y. V. Natochin ◽  
R. G. Parnova ◽  
E. I. Shakhmatova ◽  
Y. Y. Komissarchik ◽  
M. S. Brudnaya ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Water Permeability ◽  
Osmotic Water Permeability ◽  
Frog Urinary Bladder ◽  
Osmotic Water

Aquaporins in the plasma membrane of leaf callus protoplasts of Actinidia deliciosa var. deliciosa cv. Hayward

2000 ◽  
Vol 27 (1) ◽  
pp. 71
Author(s):  
Quan-Sheng Qiu ◽  
Ze-Zhou Wang ◽  
Nang Zhang ◽  
Qi-Gui Cai ◽  
Rong-Xi Jiang
Keyword(s):  
Plasma Membrane ◽  
Water Transport ◽  
Imaging System ◽  
Inhibitory Effect ◽  
Actinidia Deliciosa ◽  
Transport Activity ◽  
Water Permeability Coefficient ◽  
Osmotic Water ◽  
A Cell ◽  
Protoplast Volume

The water transport activity of Actinidia deliciosa protoplasts was determined using a cell imaging system. Results showed that the protoplast volume increased swiftly when placed in a hypoton-ic medium, and also increased with an increase in medium osmotic gradients. The osmotic water permeability coefficient (Pf) values were 0.118 × 10–3, 0.121 × 10–3, and 0.133 × 10–3 cm s–1 when the osmotic gradients were 75, 100, and 125 mosmol, respectively. The water transport activity of protoplas-ts could be inhibited by HgCl2 and stimulated by amphotericin B. Moreover, ZnCl2 and ZnSO4 had a significant inhibitory effect on the water transport activity of the protoplasts. Our results indicate that the Actinidia deliciosa protoplasts had properties typical of aquaporins, suggesting that aquaporins were present at the plasma membrane.

Inhibitory effect of phorbol ester on sodium transport in frog urinary bladder

1990 ◽  
Vol 259 (3) ◽  
pp. F425-F431
Author(s):  
T. Satoh ◽  
H. Endou
Keyword(s):  
Urinary Bladder ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Inhibitory Effect ◽  
Inhibitory Influence ◽  
Dependent Manner ◽  
Camp Accumulation ◽  
Frog Urinary Bladder ◽  
Na Transport

To confirm the role of protein kinase C (PKC) on epithelial Na transport, we studied the effects of phorbol 12-myristate 13-acetate (PMA) and dioctanoylglycerol (DiC8), activators of PKC, on short-circuit current (Isc) in frog urinary bladder and further examined the influence of sphingosine, an inhibitor of PKC, on PMA- or DiC8-modulated Isc. PMA reduced basal Isc in a dose-dependent manner, and sphingosine (10 and 100 microM) partially restored PMA-reduced Isc. On the other hand, DiC8 (5 x 10(-5) M) also reduced basal Isc, and this action was completely prevented by 100 microM sphingosine. Both PMA (4 x 10(-5) M) and DiC8 inhibited vasopressin (50 mU/ml)- and forskolin (5 x 10(-5) M)-stimulated increases in Isc. PMA (4 x 10(-5) M) also inhibited 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP)-stimulated increase in Isc. Furthermore, PMA (4 x 10(-5) M) and DiC8 (5 x 10(-5) M) inhibited vasopressin (50 mU/ml)-stimulated cAMP accumulation. DiC8 also inhibited forskolin-stimulated cAMP accumulation. These results indicate that PMA exerts inhibitory influence on Na transport mainly by its own potency of PKC activation. In addition, it is suggested that there is a cross talk in epithelial Na transport between PKC and cAMP-dependent pathway in frog urinary bladder.

Urea transport across urinary bladder and salt acclimation in toad (Bufo viridis)

1990 ◽  
Vol 258 (4) ◽  
pp. R883-R888 ◽  
Author(s):  
S. Shpun ◽  
U. Katz
Keyword(s):  
Urinary Bladder ◽  
Tap Water ◽  
Water Flux ◽  
Inhibitory Effect ◽  
Facilitated Diffusion ◽  
Urea Transport ◽  
Bufo Viridis ◽  
Salt Acclimation ◽  
Osmotic Water ◽  
Toad Bufo

The fluxes of urea across the urinary bladder of the toad Bufo viridis have been studied under conditions of acclimation to tap water or 500 mosM NaCl solution. The [14C]urea fluxes were measured simultaneously with [3H]inulin to test for nonspecific leakage. The fluxes are quite high (Ktrans = 75 x 10(-7) cm/s at 5 mmol/l urea) and are similar in either the mucosal-to-serosal or the opposite direction. “Summer” rates were five to six times higher than the “winter” rates. Antidiuretic hormone (ADH), theophylline, and forskolin increased the fluxes to variable degrees (two to five times), similar in the two acclimation conditions. Phloretin inhibited the urea fluxes by nearly 50%. 1,3-Dimethylurea and thiourea, but not acetamide, competed with the urea fluxes effectively. The fluxes of urea were not affected by the osmotic water flow, although both responded to ADH. It is concluded that urea transport across the urinary bladder of B. viridis is by facilitated diffusion through a specific pathway independent of water flux. The inhibitory effect of the structural analogues on the urea flux was affected by salt acclimation, whereas most other characteristics did not differ significantly at 5 mmol/l external urea under the two conditions of acclimation.

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.

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