PERMEABILITY AND RESPIRATION EFFECTS OF THYROIDAL HORMONES ON THE ISOLATED BLADDER OF THE TOAD BUFO BUFO

1963 ◽  
Vol 25 (4) ◽  
pp. 411-425 ◽  
Author(s):  
A. J. MATTY ◽  
K. GREEN

SUMMARY l-Thyroxine and 3,5,3′-triiodo-l-thyronine in concentrations of 10−8 m to 10−5 m were shown to increase the oxygen uptake and water transfer down an osmotic gradient in the isolated urinary bladder of Bufo bufo. The increase in water transport after treatment with thyroxine and triiodothyronine was related linearly to the log dose. The increase in O2 uptake and water movement in equimolar concentrations of thyroxine and triiodothyronine were similar but the responses to the latter were more rapid. Substitution of sodium ions by choline in the incubation medium resulted in a fall of oxygen uptake by the bladder, and a slight lowering of water loss. When thyroxine was added, oxygen uptake increased to the same extent in both media but only in sodium saline did water loss increase greatly. Specific enzyme inhibitors prevented the thyroxine-induced increase in water loss across the isolated toad bladder, indicating that metabolic energy is necessary for this alteration in permeability. Triiodothyronine and thyroxine caused an increased water loss across the isolated toad bladder when placed on either the mucosal or serosal surface. Two analogues of the thyroid hormones, 3,5,3′-triiodothyroacetic acid and 3,5,3′,5-tetraiodothyroacetic acid, caused an extremely rapid, but transient, movement of water across the bladder; their action and that of triiodothyronine and thyroxine is compared. An hypothesis is proposed tentatively to account for the mode of action of thyroxine on the permeability of the isolated toad bladder, taking into account the close relationship between increases in water permeability and metabolism, particularly that involving sodium transport.

1964 ◽  
Vol 28 (2) ◽  
pp. 205-211 ◽  
Author(s):  
K. GREEN ◽  
A. J. MATTY

SUMMARY Thyroxine at 10−6m concentration enhances water movement from the mucosal to the serosal surface of the isolated toad bladder in the absence of an osmotic gradient. It is suggested that this is caused by the effect of thyroxine on sodium transport which creates a driving force for the increased water movement. Thyroxine caused this effect when applied on either side of the membrane, but was more effective when applied to the serosal surface. Incubation of different bladders successively in the same triiodothyronine solution indicated that triiodothyronine may be rapidly utilized. A mixture of thyroxine and triiodothyronine caused a diphasic effect on water loss down an osmotic gradient. The analogues tetraiodothyroproprionic acid and tetraiodothyroformic acid had no effect on water movement down an osmotic gradient across the isolated toad bladder nor did they affect oxygen uptake or sodium transport. The results support the concept that thyroxine and triiodothyronine act on permeability processes in and across cell membranes.


2000 ◽  
Vol 1 (1) ◽  
pp. 10-14
Author(s):  
Sulaiman Ibrahim

ABSTRACT. Studies have been made on the isolated urinary bladder of the toad, Bufo marinus, in an attempt to investigate the effect of vasopressin on the permeability of water from mucosal surface to serosal surface of the toad bladder. The method adapted was that described by Bentley ( 1 ). The bilobed bladder of the toad is devided into two separate sacs. Each of the sacs is filled with a dilute Ringers solution and then immersed in aerated isotonic Ringers solution. The rate of water loss along the imposed osmotic gradient is estimated by weighing the sacs in air at 30 minute intervals and nothing the weight  loss in that time period. In most studies one bladder sac serves as a control for the contra lateral experimental obtained from the same animal. Osmotic flow of water is negligible in both sacs during the initial control periods. However, the addition of vasopressin to the solution bathing the serosal surface of the membrane result in a market increase in net water movement. The effect is readily reversed by rinsing the bladder and adding hormone free Ringgers solution to the serosal surface. Characteristically no response is elicited by addition of hormone to the mucosal bathing solution.


1975 ◽  
Vol 67 (1) ◽  
pp. 119-125
Author(s):  
P. J. BENTLEY

SUMMARY The electrical potential difference and short-circuit current (scc, reflecting active transmural sodium transport) across the toad urinary bladder in vitro was unaffected by the presence of hypo-osmotic solutions bathing the mucosal (urinary) surface, providing that the transmural flow of water was small. Vasopressin increased the scc across the toad bladder (the natriferic response), but this stimulation was considerably reduced in the presence of a hypo-osmotic solution on the mucosal side, conditions under which water transfer across the membrane was also increased. This inhibition of the natriferic response did not depend on the direction of the water movement, for if the osmotic gradient was the opposite way to that which normally occurs, the response to vasopressin was still reduced. The natriferic response to cyclic AMP was also inhibited in the presence of an osmotic gradient. Aldosterone increased the scc and Na+ transport across the toad bladder but this response was not changed when an osmotic gradient was present. The physiological implications of these observations and the possible mechanisms involved are discussed.


1961 ◽  
Vol 22 (1) ◽  
pp. 95-100 ◽  
Author(s):  
P. J. BENTLEY

SUMMARY 1. If the osmotic gradient is favourable vasopressin increases the rate of water movement across the bladder of the toad from the serosal to the epithelial side, which is the opposite direction to that seen physiologically. 2. Water transfer down an osmotic gradient is 1·8 times more rapid towards the serosal than towards the epithelial side. Vasopressin increases this difference so that water is moving 4·9 times as rapidly to the serosal side. Iodoacetate reduces this effect of vasopressin. 3. If water is moving down an osmotic gradient towards the anode, a higher electric current increases the water movement in the presence, but not in the absence, of vasopressin. If water movement is taking place towards the cathode an increased current has no effect. 4. With vasopressin present, absence of sodium on the epithelial side of the bladder reduces water transfer down an osmotic gradient towards the serosal side, but has no effect on water movement down an osmotic gradient in the opposite direction.


1962 ◽  
Vol 45 (5) ◽  
pp. 905-919 ◽  
Author(s):  
Richard M. Hays ◽  
Alexander Leaf

Measurements of diffusion permeability and of net transfer of water have been made across the isolated urinary bladder of the toad, Bufo marinus, and the effects thereon of mammalian neurohypophyseal hormone have been examined. In the absence of a transmembrane osmotic gradient, vasopressin increases the unidirectional flux of water from a mean of 340 to a mean of 570 µl per cm2 per hour but the net water movement remains essentially zero. In the presence of an osmotic gradient but without hormone net transfer of water remains very small. On addition of hormone large net fluxes of water occur; the magnitude of which is linearly proportional to the osmotic gradient. The action of the hormone on movement of water is not dependent on the presence of sodium or on active transport of sodium. Comparison of the net transport of water and of unidirectional diffusion permeability of the membrane to water indicates that non-diffusional transport must predominate as the means by which net movement occurs in the presence of an osmotic gradient. An action of the hormone on the mucosal surface of the bladder wall is demonstrated. The effects of the hormone on water movement are most simply explained as an action to increase the permeability and porosity of the mucosal surface of the membrane.


Author(s):  
Shi-wen Zhou ◽  
Jing-yu Quan ◽  
Zi-wei Li ◽  
Ge Ye ◽  
Zhuo Shang ◽  
...  

2006 ◽  
Vol 454 (1) ◽  
pp. 101-113 ◽  
Author(s):  
Nadja Møbjerg ◽  
Andreas Werner ◽  
Sofie M. Hansen ◽  
Ivana Novak

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