A histochemical study of the toad urinary bladder

Keller, Albert R.

doi:10.1002/ar.1091470308

Cited by 42 publications

(26 citation statements)

References 36 publications

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“…4), indicating a high concentration of carbohydrates. The luminal cell surface also shows silver methenamine reaction product consistent with the suggestion that the source of the membrane " f u z z " is the granules (Choi, 1963;Keller, 1963;Masur et al, 1972).…”

Section: Exocytosissupporting

confidence: 82%

Quantitative analysis of exocytosis and endocytosis in the hydroosmotic response of toad bladder

1980

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This study concerns the timing and magnitude of exocytosis and endocytosis in the granular cells of toad bladder during the hydroosmotic response to antidiuretic hormone. Granule exocytosis at the luminal cell surface is extensive within 5 min of the administration of a physiological dose of hormone. Hydroosmosis becomes detectable during this time period. The amount of membrane added to the luminal surface by exocytosis during 60 min of exposure to hormone can be of the same order of magnitude as the extent of the luminal plasma membrane. Endocytosis, demonstrated by peroxidase uptake from the luminal surface, becomes extensive during the period 15-45 min after hormone administration. Thus, maximal endocytic activity occurs later than the period of most extensive exocytosis and seems to correlate with the onset of the decline in water movement. The amount of membrane retrieved from the luminal surface by endocytosis during 60 min of stimulation is at least three quarters of that added by exocytosis. The bulk membrane movement in ADH stimulated preparations does not require the presence of an osmotic gradient. Colchicine inhibits the hydroosmotic response, the exocytosis of granules, and endocytosis at the luminal surface. These results strengthen our view that the bulk circulation of membrane at the cell surface, via exocytosis and endocytosis, is closely related to the permeability changes occurring at the surface.

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Section: Exocytosissupporting

confidence: 82%

Quantitative analysis of exocytosis and endocytosis in the hydroosmotic response of toad bladder

1980

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“…Sodium transport across the toad bladder is inhibited by ouabain (Bonting & Canady, 1964), an action mediated by inhibition of 322 P. J. BENTLEY AMILORIDE AND TOAD BLADDER ATPase (Skou, 1965) which has been located histochemically at the serosal border of the bladder epithelial cells (Keller, 1963) where ouabain is also considered to act (Herrera, 1966). Thus the effects of ouabain and amiloride in relation to the mucosal action of amphotericin B may provide information relevant to their sites of action.…”

Section: Resultsmentioning

confidence: 99%

Amiloride: a potent inhibitor of sodium transport across the toad bladder

Bentley¹

1968

The Journal of Physiology

387

151

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SUMMARY1 Amiloride inhibits Na transport and short-circuit current (SCC) across the toad bladder. It is 1000 times more active at the mucosal than serosal surface. The lowest effective concentration was 10-7 M.2. The inhibition was non-competitive with the sodium on the mucosal side of the bladder.3. Vasopressin, cyclic adenosine monophosphate (AMP) and aldosterone increased Na transport and SCC across the bladder and these effects were inhibited by amiloride.4. The antagonism of amiloride, for vasopressin was non-competitive.5. Amphotericin B also increases Na transport across the bladder but its action was not changed by amiloride.6. Amiloride was without effects on SCC and diffusion potentials in bladders metabolically inhibited with CN-and iodoacetic acid (IAA).7. Neither plasma albumin, Ca2+ nor adenosine triphosphate (ATP) altered the effects of amiloride.8. The only structural analogue of amiloride found to reduce SCC similarly was guanidine which was 1000 times less active. Pyrazine and a substituted pyrazine analogue were without effect. Neither guanidine nor the substituted pyrazine compound were competitive with amiloride.9. Amiloride had no effect on the osmotic permeability of the toad bladder either in the presence or absence of vasopressin.10. Na transport across the toad colon was also reduced by 10-5 M amiloride at the mucosal surface.11. The possible mechanism of action of amiloride is discussed.

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“…There is indirect evidence from previous studies that two compartments of cyclic AMP exist within one cell type. For instance, sodium transport responsive to ADH (and therefore cyclic AMP) occurs in the granular cells, the cells which make up some 85% of the mucosal epithelial cell layer (17,18). This is because membranes of the granular cells make up more than 90% of the surface area of the apical side of the bladder (19).…”

Section: Effects Of Pge1 On Adh-stimulated Sodium Transportmentioning

confidence: 99%

Stimulation of osmotic water flow in toad bladder by prostaglandin E1. Evidence for different compartments of cyclic AMP.

Flores¹,

Witkum²,

Beckman³

et al. 1975

J. Clin. Invest.

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A B S T R A CT The effect of prostaglandin Ei (PGEi) on osmotic water flow across toad bladder and cyclic AMP content of the mucosal epithelial cells has been determined under basal conditions and in the presence of either theophylline or antidiuretic hormone (ADH). Under basal conditions and with PGE, concentrations from 10 to 10' M no evidence of stimulation of water flow was observed, and with 10' M PGEi a significant inhibition was found. Cyclic AMP content under control conditions was 8 pmol/mg protein. It was 9 at 10' M PGEi, 13 at 10' M, 16 at 10' M, and 23 at 10' M. In the presence of theophylline, 10' and 10V M PGE1 inhibited the theophylline-induced water flow as expected. In contrast, 10' and adenylate cyclase controlling water flow. Thus the increase in cyclic AMP content in response to PGE, is not derived from this enzyme. Thus the stimulation of water flow by PGE1 in the presence of theophylline is thought to be caused by cyclic AMP spilling over from one compartment to the water flow compartment. No evidence was obtained to directly suggest spillover into the sodium transport compartment. Furthermore evidence is discussed to suggest that most of the cyclic AMP generated in the tissue does not originate from the enzyme controlling sodium transport. As cyclic AMP-stimulated water flow and sodium transport are thought to occur in one cell type, the granular cells, distinct pools of cyclic AMP are thought to be present in one and the same cell type. Thus one pool controls water flow and one controls sodium transport. With high concentrations of PGE1 in the presence of theophylline or high concentrations of ADH, the adenylate cyclase responsible for water flow is inhibited. However, PGEi can stimulate a tissue adenylate cyclase to sufficiently high levels that cyclic AMP spills over into the "water flow compartment" and thus stimulates water flow.

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A histochemical study of the toad urinary bladder

Cited by 42 publications

References 36 publications

Quantitative analysis of exocytosis and endocytosis in the hydroosmotic response of toad bladder

Quantitative analysis of exocytosis and endocytosis in the hydroosmotic response of toad bladder

Amiloride: a potent inhibitor of sodium transport across the toad bladder

Stimulation of osmotic water flow in toad bladder by prostaglandin E1. Evidence for different compartments of cyclic AMP.

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