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.

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

scholarly journals Very high water permeability in vasopressin-induced endocytic vesicles from toad urinary bladder.

1989 ◽  
Vol 94 (6) ◽  
pp. 1101-1115 ◽  
Author(s):  
L B Shi ◽  
A S Verkman
Keyword(s):  
Urinary Bladder ◽  
Water Permeability ◽  
Time Course ◽  
Toad Urinary Bladder ◽  
Stopped Flow ◽  
Osmotic Water Permeability ◽  
Luminal Membrane ◽  
Osmotic Water ◽  
Group A ◽  
Endocytic Vesicles

The regulation of transepithelial water permeability in toad urinary bladder is believed to involve a cycling of endocytic vesicles containing water transporters between an intracellular compartment and the cell luminal membrane. Endocytic vesicles arising from luminal membrane were labeled selectively in the intact toad bladder with the impermeant fluid-phase markers 6-carboxyfluorescein (6CF) or fluorescein-dextran. A microsomal preparation containing labeled endocytic vesicles was prepared by cell scraping, homogenization, and differential centrifugation. Osmotic water permeability was measured by a stopped-flow fluorescence technique in which microsomes containing 50 mM mannitol, 5 mM K phosphate, pH 8.5 were subject to a 60-mM inwardly directed gradient of sucrose; the time course of endosome volume, representing osmotic water transport, was inferred from the time course of fluorescence self-quenching. Endocytic vesicles were prepared from toad bladders with hypoosmotic lumen solution treated with (group A) or without (group B) serosal vasopressin at 23 degrees C, and bladders in which endocytosis was inhibited by treatment with vasopressin at 0-2 degrees C (group C), or with vasopressin plus sodium azide at 23 degrees C (group D). Stopped-flow results in all four groups showed a slow rate of 6CF fluorescence decrease (time constants 1.0-1.7 s for exponential fit) indicating a component of nonendocytic 6CF entrapment into sealed vesicles. However, in vesicles from group A only, there was a very rapid 6CF fluorescence decrease (time constant 9.6 +/- 0.2 ms, SEM, 18 separate preparations) with an osmotic water permeability coefficient (Pf) of greater than 0.1 cm/s (18 degrees C) and activation energy of 3.9 +/- 0.8 kcal/mol (16 kJ/mol). Pf was inhibited reversibly by greater than 60% by 1 mM HgCl2. The rapid fluorescence decrease was absent in vesicles in groups B, C, and D. These results demonstrate the presence of functional water transporters in vasopressin-induced endocytic vesicles from toad bladder, supporting the hypothesis that water channels are cycled to and from the luminal membrane and providing a functional marker for the vasopressin-sensitive water channel. The calculated Pf in the vasopressin-induced endocytic vesicles is the highest Pf reported for any biological or artificial membrane.

Diluting segment in avian kidney. II. Water and chloride transport

1986 ◽  
Vol 250 (3) ◽  
pp. R341-R347 ◽  
Author(s):  
T. Miwa ◽  
H. Nishimura
Keyword(s):  
Water Permeability ◽  
Chloride Transport ◽  
Arginine Vasotocin ◽  
Osmotic Gradient ◽  
Thick Ascending Limb ◽  
Osmotic Water Permeability ◽  
Diluting Segment ◽  
Henle's Loop ◽  
Osmotic Water ◽  
Avian Kidney

The mammalian-type nephrons of avian kidneys contain a Henle's loop that runs parallel to the collecting ducts and the vasa recta. Thus we examined whether the thick ascending limb (TAL) of Henle's loop of the avian kidney acts as a diluting segment by measuring water and Cl transport in the isolated and perfused TAL of the quail, Coturnix coturnix. The TAL showed a lumen-positive transepithelial voltage (Vt) (+9.4 +/- 0.4 mV, n = 28). Net water flux (Jv) was nearly zero when the TAL was perfused and bathed with isosmotic solution. When the osmotic gradient was imposed, Jv increased only slightly, and thus the osmotic water permeability (Lp) was low. Arginine vasotocin (AVT) added to the hyperosmotic bath did not alter either Jv, Lp, or Vt. Cl efflux (lumen to bath, 370.4 +/- 27.7 peq X mm-1 X min-1) was higher than Cl influx (bath to lumen, 98.6 +/- 14.3 peq X mm-1 X min-1) when measured in the different tubules. AVT showed no effect on Cl efflux. These results indicate that in the TAL of the quail osmotic water permeability is low while net Cl reabsorption is present, suggesting that the TAL functions as a diluting segment.

Endothelin-1 inhibits AVP-stimulated osmotic water permeability in rat inner medullary collecting duct

1991 ◽  
Vol 261 (6) ◽  
pp. F951-F956 ◽  
Author(s):  
R. Oishi ◽  
H. Nonoguchi ◽  
K. Tomita ◽  
F. Marumo
Keyword(s):  
Water Permeability ◽  
Collecting Duct ◽  
Renal Plasma Flow ◽  
Inhibitory Effect ◽  
Osmotic Water Permeability ◽  
Camp Generation ◽  
Osmotic Water ◽  
Collecting Ducts ◽  
Medullary Collecting Duct

Endothelin causes diuresis despite an accompanying decrease in glomerular filtration rate and renal plasma flow. Binding sites for endothelin are located not only in glomeruli but also in the inner medulla, possibly in inner medullary collecting ducts (IMCD). To determine whether endothelin has a direct tubular effect, effects of endothelin on water and urea transport were investigated using isolated microperfusion of rat IMCD segments in vitro. Endothelin, at 10(-10) and 10(-8) M, reversibly inhibited 10(-11) M arginine vasopressin (AVP)-stimulated osmotic water permeability (Pf) by 18 and 24%, respectively. Endothelin (10(-8) M) also inhibited Pf by 23% in the presence of a much higher dose of AVP (10(-9) M), whereas endothelin had no effect on Pf in the absence of AVP. On the other hand, 10(-8) M endothelin did not inhibit Pf stimulated by 10(-3) M dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP). Endothelin had no inhibitory effect on AVP-stimulated urea permeability. These data suggest that endothelin can cause diuresis by inhibiting AVP-stimulated Pf in IMCD and that the site of action is previous to cAMP generation.

Prostaglandin-dependent osmotic water permeability of the frog and trout urinary bladder

1998 ◽  
Vol 121 (1) ◽  
pp. 59-66 ◽  
Author(s):  
Yu.V. Natochin ◽  
E.I. Shakhmatova ◽  
Ya.Yu. Komissarchik ◽  
E.S. Snigirevskaya ◽  
N.P. Prutskova ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Water Permeability ◽  
Osmotic Water Permeability ◽  
Osmotic Water

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.

Osmotic water permeability of rat intestinal brush border membrane vesicles: involvement of aquaporin-7 and aquaporin-8 and effect of metal ions

2007 ◽  
Vol 85 (6) ◽  
pp. 675-684 ◽  
Author(s):  
Simona Tritto ◽  
Giulia Gastaldi ◽  
Sergey Zelenin ◽  
Monica Grazioli ◽  
Maria Novella Orsenigo ◽  
...  
Keyword(s):  
Small Intestine ◽  
Epithelial Cells ◽  
Water Permeability ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Water Movement ◽  
Membrane Vesicles ◽  
Osmotic Water Permeability ◽  
Transfected Cells ◽  
Osmotic Water

Water channels AQP7 and AQP8 may be involved in transcellular water movement in the small intestine. We show that both AQP7 and AQP8 mRNA are expressed in rat small intestine. Immunoblot and immunohistochemistry experiments demonstrate that AQP7 and AQP8 proteins are present in the apical brush border membrane of intestinal epithelial cells. We investigated the effect of several metals and pH on the osmotic water permeability (Pf) of brush border membrane vesicles (BBMVs) and of AQP7 and AQP8 expressed in a cell line. Hg2+, Cu2+, and Zn2+ caused a significant decrease in the BBMV Pf, whereas Ni2+ and Li+ had no effect. AQP8-transfected cells showed a reduction in Pf in the presence of Hg2+ and Cu2+, whereas AQP7-transfected cells were insensitive to all tested metals. The Pf of both BBMVs and cells transfected with AQP7 and AQP8 was not affected by pH changes within the physiological range, and the Pf of BBMVs alone was not affected by phlorizin or amiloride. Our results indicate that AQP7 and AQP8 may play a role in water movement via the apical domain of small intestine epithelial cells. AQP8 may contribute to the water-imbalance-related clinical symptoms apparent after ingestion of high doses of Hg2+ and Cu2+.

Relation of ADH effects to altered membrane fluidity in toad urinary bladder

1981 ◽  
Vol 240 (1) ◽  
pp. F63-F69
Author(s):  
W. A. Kachadorian ◽  
J. Muller ◽  
S. Rudich ◽  
V. A. DiScala
Keyword(s):  
Urinary Bladder ◽  
Membrane Fluidity ◽  
Water Permeability ◽  
Membrane Lipids ◽  
Granular Cell ◽  
Toad Urinary Bladder ◽  
Osmotic Water Permeability ◽  
Intramembranous Particle ◽  
Luminal Membrane ◽  
Osmotic Water

Membrane fluidity, urea permeability, and osmotic water permeability in toad urinary bladder are regularly enhanced by antidiuretic hormone (ADH). In addition, organized intramembranous particle aggregates, which correlate specifically with hormonally stimulated water permeability, are found in granular cell luminal membranes consequent to ADH stimulation. In this investigation ADH-stimulated changes in urea and osmotic water permeability and luminal membrane aggregates at room temperature (24.8 +/- 0.4 degrees C) and in the cold 10.6 +/- 0.2 degrees) were compared with corresponding changes in membrane fluidity, as assessed by n-butyramide permeability. Although a critical level of membrane fluidity is undoubtedly required, the occurrence of aggregates in the luminal membrane is independent of an accompanying hormonally induced change of membrane fluidity. ADH-stimulated osmotic water permeability in toad bladder is also independent of the coincident change in membrane fluidity, and as a process almost certainly involves membrane channels, not a solubility-diffusion process through membrane lipids. For ADH-stimulated transbladder urea movement, channels seem to be involved as well, and the change induced in membrane fluidity by ADH could be an underlying factor in their formation.

Sign in / Sign up

Export Citation Format

Share Document