Temperature dependence of ADH-induced water flow and intramembranous particle aggregates in toad bladder

Science ◽  
1979 ◽  
Vol 205 (4409) ◽  
pp. 910-913 ◽  
Author(s):  
W. Kachadorian ◽  
J Muller ◽  
S. Rudich ◽  
V. DiScala
Keyword(s):  
Temperature Dependence ◽  
Water Flow ◽  
Toad Bladder ◽  
Intramembranous Particle ◽  
Particle Aggregates ◽  
Intramembranous Particle Aggregates

Possible roles for microtubules and microfilaments in ADH action on toad urinary bladder

1979 ◽  
Vol 236 (1) ◽  
pp. F14-F20 ◽  
Author(s):  
W. A. Kachadorian ◽  
S. J. Ellis ◽  
J. Muller
Keyword(s):  
Water Flow ◽  
Cytochalasin B ◽  
Toad Urinary Bladder ◽  
Intramembranous Particle ◽  
Luminal Membrane ◽  
Osmotic Water ◽  
Particle Aggregates ◽  
Aggregation Phenomenon ◽  
Osmotic Water Flow ◽  
Intramembranous Particle Aggregates

Intramembranous particle aggregates in the luminal membrane of toad bladder granular cells after vasopressin stimulation have been found to correlate closely and specifically with induced alterations of water permeability. Roles for microtubules and microfilaments in mediating the latter response have been proposed on the basis of studies involving colchicine and cytochalasin B, respectively. In the present investigation the effects of these agents on both initiating and sustaining vasopressin-induced osmotic water flow and the particle aggregation phenomenon were studied. The results indicate that during initiation the aggregation and water flow responses to vasopressin are each colchicine- and cytochalasin B-sensitive and that these sensitivities can be wholly additive. However, after full vasopressin stimulation is established, the same responses demonstrate sensitivity only to cytochalasin B, not to colchicine. The findings, therefore, suggest that microtubules and microfilaments may be independently necessary for the initiation of the aggregation and water flow responses to vasopressin, and that microfilaments, but not microtubules, are required for their maintenance.

Effects of cellular acidification on ADH-induced intramembrane particle aggregates

1984 ◽  
Vol 246 (1) ◽  
pp. C157-C159 ◽  
Author(s):  
M. Parisi ◽  
J. Bourguet
Keyword(s):  
Membrane Surface ◽  
Water Flux ◽  
Medium Ph ◽  
Intramembranous Particle ◽  
Intramembrane Particle ◽  
Cyclic Monophosphate ◽  
Particle Aggregates ◽  
Camp Levels ◽  
Cellular Acidification ◽  
Intramembranous Particle Aggregates

8-Bromoadenosine 3',5'-cyclic monophosphate [an analogue of adenosine 3',5'-cyclic monophosphate (cAMP), the intracellular mediator for antidiuretic hormone (ADH) action] induces, in frog urinary bladder, an increase in water permeability that is rapidly and reversibly inhibited by cellular acidification. The effect of CO2 bubbling on the simultaneously observed intramembranous particle aggregates, which probably represent water channels, depended on the time that elapsed after changing medium pH: 3 min of CO2 bubbling depressed the water flux by 70%, whereas the membrane surface occupied by the aggregates remained unchanged. On the contrary, after 9-15 min of CO2 bubbling, both the water flux and the surface area occupied by the aggregates were strongly reduced. These results can be interpreted by accepting two post-cAMP levels of action for cellular acidification: 1) the channels themselves that, as previously suggested by ADH experiments at low temperature, would shift their structure from an "open" to a "closed" state, and 2) the mechanism that controlled the aggregates' plug in and removal.

ADH-induced water permeability and particle aggregates: alteration by a synthetic estrogen

1991 ◽  
Vol 261 (1) ◽  
pp. F144-F152 ◽  
Author(s):  
G. Calamita ◽  
Y. Le Guevel ◽  
J. Bourguet
Keyword(s):  
Urinary Bladder ◽  
Water Flow ◽  
Water Permeability ◽  
Glucose Transporter ◽  
Apical Membrane ◽  
Selective Inhibition ◽  
Synthetic Estrogen ◽  
Permeability Changes ◽  
Particle Aggregates ◽  
Amphibian Urinary Bladder

In the amphibian urinary bladder, the increase in water permeability induced by antidiuretic hormone (ADH) is accompanied by the appearance of apical intramembrane particle (IMP) aggregates that are believed to contain specific channels for water. In a previous work, we have shown that 3,3'-diallyldiethylstilbestrol (DADES), a synthetic estrogen which is a blocker of the glucose transporter, also inhibits the hydrosmotic response to ADH in the bladder. Our aim in the present study was to analyze the alterations of the membrane fine structure further and to correlate them with the water permeability changes. The results point to a selective inhibition of the ADH-induced net water flow, probably due to an interference with one of the last steps of the response to the hormone. This inhibition is associated with an increase in the density of the apical IMP aggregates, which are thus probably not operational. The resting net water flow is not inhibited and, surprisingly, typical IMP aggregates are frequently observed in the apical membrane after DADES treatment. The compound also induces the appearance of unusual loose IMP clusters that can only be seen on the apical membrane of the granular cells and that share several ultrastructural similarities with the ADH-induced aggregates. These results suggest that 1) apical DADES treatment stimulates the insertion of IMP aggregates in the apical membrane of the urinary bladder and 2) DADES inhibits the ADH-induced water flow by interfering with the aggregates and thus probably by blocking the specific water channels.

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