Effects of vasopressin on hyaluronate hydrolase activities and water permeability in the frog urinary bladder

2001 ◽  
Vol 443 (1) ◽  
pp. 72-77 ◽  
Author(s):  
L. Ivanova ◽  
N. Melidi
Keyword(s):  
Urinary Bladder ◽  
Water Permeability ◽  
Frog Urinary Bladder

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

REGULATION BY ADH AND CELLULAR OSMOLARITY OF WATER PERMEABILITY IN FROG URINARY BLADDER: A TIME COURSE STUDY

1981 ◽  
Vol 372 (1 Hormonal Regu) ◽  
pp. 144-162 ◽  
Author(s):  
M. Parisi ◽  
P. Ripoche ◽  
G. Prevost ◽  
J. Bourguet
Keyword(s):  
Urinary Bladder ◽  
Water Permeability ◽  
Time Course ◽  
Frog Urinary Bladder ◽  
Time Course Study

Cellular pH and water permeability control in frog urinary bladder a possible action on the water pathway

1981 ◽  
Vol 648 (2) ◽  
pp. 267-274 ◽  
Author(s):  
Mario Parisi ◽  
Ricardo Montoreano ◽  
Jacques Chevalier ◽  
Jacques Bourguet
Keyword(s):  
Urinary Bladder ◽  
Water Permeability ◽  
Frog Urinary Bladder ◽  
Water Pathway

scholarly journals The Effect of Hypertonic Media on Water Permeability of Frog Urinary Bladder

1973 ◽  
Vol 61 (1) ◽  
pp. 110-124 ◽  
Author(s):  
P. Ripoche ◽  
J. Bourguet ◽  
M. Parisi
Keyword(s):  
Epithelial Cells ◽  
Urinary Bladder ◽  
Cyclic Amp ◽  
Antidiuretic Hormone ◽  
Water Permeability ◽  
Prostaglandin E1 ◽  
Physiological State ◽  
Solution Temperature ◽  
Bathing Solution ◽  
Frog Urinary Bladder

The frog urinary bladder undergoes, in some conditions, a marked increase of its water permeability when incubated in hypertonic media. This increase was observed with various nonpermeant solutes. It seems to result from the shrinkage of an osmo-sensitive compartment of the tissue, probably the epithelial cells. Many similarities were found between this effect and the physiological increase in water permeability (hydrosmotic response) elicited by antidiuretic hormone (ADH): both were dependent on the physiological state of the animals, and although the response was slower after hyperosmolar than after hormonal challenge, the patterns of response were similar, and in both cases markedly dependent on bathing solution temperature. Norepinephrine and prostaglandin E1, which in this tissue reduce the hydrosmotic action of ADH, presumably by inhibiting the adenyl cylase also reduced the effect of hyperosmolarity. Conversely this effect was potentiated by incubation in the presence of oxytocin, exogenous cyclic AMP, and theophylline, conditions in which the intracellular concentration of cyclic AMP is increased. These data demonstrate that the response to hyperosmolarity is elicited, at least partly, by mechanisms also involved in the physiological hydrosmotic response to ADH.

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.

scholarly journals Intracellular calcium as a modulator of transepithelial permeability to water in frog urinary bladder.

1978 ◽  
Vol 76 (3) ◽  
pp. 787-791 ◽  
Author(s):  
M A Hardy
Keyword(s):  
Urinary Bladder ◽  
Intracellular Calcium ◽  
Water Permeability ◽  
Calcium Concentration ◽  
Water Movement ◽  
Water Flux ◽  
Frog Urinary Bladder ◽  
A 23187 ◽  
Dose Dependent Fashion ◽  
Dose Dependent

The divalent cation ionophore A 23187 was used to evaluate the action of intracellular calcium on net transepithelial water movement across the isolated frog urinary bladder. Incubation with the ionophore increases the net basal water flux in a dose-dependent fashion but independent of the extracellular calcium concentration. Bladders pretreated with A 23187 and exposed thereafter to an increase in calcium concentration exhibit a water permeability that under certain conditions can be comparable to that achieved with antidiuretic hormone (ADH). Lowering the serosal calcium at the peak of the hydrosmotic responses to both ADH and A 23187 inhibited the maintenance of the net water flux. The action of a supramaximal dose of ADH is blunted in bladders pretreated with A 23187, while the hydrosmotic effects of a submaximal dose are enhanced when the ionophore is added together with the hormone. The results show that an increase in transepithelial water movement can be triggered by calcium and that serosal calcium is needed to sustain the response. This hydrosmotic response may be dependent upon the rate at which intracellular calcium concentrations change and on the absolute concentration attained. It is suggested that calcium is involved in the action of ADH on water permeability and may act as a modulator of the hydrosmotic response.

Probenecid: Effects on water permeability in frog urinary bladder

1972 ◽  
Vol 255 (1) ◽  
pp. 91-97 ◽  
Author(s):  
P. Ripoche ◽  
M. Parisi ◽  
J. Bourguet
Keyword(s):  
Urinary Bladder ◽  
Water Permeability ◽  
Frog Urinary Bladder
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