The role of intercellular channels in the transepithelial transfer of water and sodium in the frog urinary bladder

1971 ◽  
Vol 4 (1) ◽  
pp. 124-147 ◽  
Author(s):  
S. Jard ◽  
J. Bourguet ◽  
p. Favard ◽  
N. Carasso
Keyword(s):  
Urinary Bladder ◽  
Frog Urinary Bladder ◽  
Intercellular Channels

scholarly journals Role of prostaglandin E2 in regulation of low and high water osmotic permeability in frog urinary bladder

1997 ◽  
Vol 1356 (2) ◽  
pp. 160-170 ◽  
Author(s):  
Rimma G Parnova ◽  
Elena I Schakhmatova ◽  
Svetlana A Plesneva ◽  
Elena V Getmanova ◽  
Evgeny V Korolev ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Prostaglandin E2 ◽  
High Water ◽  
Frog Urinary Bladder ◽  
Osmotic Permeability

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.

The hydroosmotic response of frog urinary bladder to serosal hypertonicity is dependent on adenylate cyclase for its maintenance and affected by [Cl−]o changes

2006 ◽  
Vol 291 (1) ◽  
pp. R213-R223 ◽  
Author(s):  
Ann T. Hanna-Mitchell ◽  
Elizabeth M. Gebruers
Keyword(s):  
Urinary Bladder ◽  
Adenylate Cyclase ◽  
Adrenergic Receptors ◽  
Inhibitory Action ◽  
Channel Blocker ◽  
Rana Temporaria ◽  
Frog Urinary Bladder ◽  
Cell Shrinkage ◽  
Hypertonic Medium

The role of adenylate cyclase (AC) in the maintenance of the hydroosmotic response to serosal hypertonicity (SH) in anuran urinary bladder is disputed. In this study, norepinephrine (NE) significantly reversed the hydroosmotic response of Rana temporaria bladders in hypertonic medium (330 mosmol/kgH2O). The reversal was inhibited by yohimbine but was unaffected by prazosin and propranolol, indicating that NE action was mediated via α2-adrenergic receptors. Preincubation of bladders with indomethacin did not interfere with the inhibitory action of NE, contraindicating a role for prostaglandins. The SH hydroosmotic response was abolished in the presence of 5- n-ethyl- N-isopropyl amiloride (EIPA), but the antidiuretic hormone (ADH) hydroosmotic response was not. EIPA inhibits Na+/H+, known to be activated by cell shrinkage. An investigation of the anionic requirement of the SH hydroosmotic response revealed that replacement of bath Cl− with the nonpermeable anion gluconate reversibly abolished this response. In contrast, the hydroosmotic response to ADH was unaffected by Cl− removal; however, when Cl− was absent, it was no longer augmented in hypertonic bath. The SH response was inhibited by the Cl− channel blocker 5-nitro-2-(3-phenylpropylamino)benzoate but not by the Na/K/2Cl inhibitor bumetanide. Our results show that not only the onset but also the maintenance of the SH hydroosmotic response is dependent on AC activity and does not differ in this respect to the ADH hydroosmotic response. The effect of modifying extracellular Cl− concentration, suggests that this anion, possibly functionally linked with Na+/H+ activity, may be involved in invoking the SH hydroosmotic response in anuran urinary bladder.

Role of PKC isozymes in water transport in toad urinary bladder

1991 ◽  
Vol 49 ◽  
pp. 302-303
Author(s):  
A.J. Mia ◽  
L.X. Oakford ◽  
T. Yorio
Keyword(s):  
Urinary Bladder ◽  
Apical Membrane ◽  
Membrane Surface ◽  
Protein A ◽  
Cell Types ◽  
Leukemic Cells ◽  
Toad Urinary Bladder ◽  
Pkc Isozymes ◽  
Antibody Labeling

Protein kinase C (PKC) isozymes, when activated, are translocated to particulate membrane fractions for transport to the apical membrane surface in a variety of cell types. Evidence of PKC translocation was demonstrated in human megakaryoblastic leukemic cells, and in cardiac myocytes and fibroblasts, using FTTC immunofluorescent antibody labeling techniques. Recently, we reported immunogold localizations of PKC subtypes I and II in toad urinary bladder epithelia, following 60 min stimulation with Mezerein (MZ), a PKC activator, or antidiuretic hormone (ADH). Localization of isozyme subtypes I and n was carried out in separate grids using specific monoclonal antibodies with subsequent labeling with 20nm protein A-gold probes. Each PKC subtype was found to be distributed singularly and in discrete isolated patches in the cytosol as well as in the apical membrane domains. To determine if the PKC isozymes co-localized within the cell, a double immunogold labeling technique using single grids was utilized.

THE ROLE OF THE MOTHER IN 131I METABOLISM OF SUCKING AND WEANLING RATS

1965 ◽  
Vol 43 (3) ◽  
pp. 431-436 ◽  
Author(s):  
M. Samel ◽  
A. Caputa
Keyword(s):  
Urinary Bladder ◽  
In Utero ◽  
The State ◽  
Newborn Rats ◽  
Weanling Rats ◽  
Immature Rats ◽  
Other Substances ◽  
Old Rats

In newborn rats the mother provokes the emptying of the urinary bladder by stimulating the perineum with her tongue. The possibility that mothers may thereby ingest the urine of their young has been studied by means of 131I on nine litters of rats aged 10 to 29 days. The results indicate that a considerable quantity of 131I administered intraperitoneally to 10- and 18-day-old rats, which were then reunited with their mothers for 4 hours, reappears in the organism of uninjected nurslings after passing through the organism of the mother. The amount of 131I transferred from injected rats into the bodies of isolated uninjected rats of the same litter decreased during the period of weaning. The observed recirculation of 131I between immature rats and their mothers in both directions may represent a saving mechanism which might include several other substances and would compensate for their loss via the milk, and suggests a new aspect of maternal–neonatal interrelationship which appears as a continuation of the state existing in utero.

THE ROLE OF INTERLEUKIN-6 ON THE CONTRACTILE RESPONSES OF RAT URINARY BLADDER

2006 ◽  
Vol 5 (2) ◽  
pp. 79
Author(s):  
S.C. Myung ◽  
M.Y. Lee ◽  
M.K. Lee ◽  
S.H. Ahn ◽  
T.H. Kim ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Interleukin 6 ◽  
Rat Urinary Bladder ◽  
Contractile Responses
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