Vasopressin-Induced Changes in the Toad Urinary Bladder Epithelial Surface

Davis, Walter L.; Goodman, David B. P.; Martin, J. Holmes; Matthews, James L.; Rasmussen, Howard

doi:10.1083/jcb.61.2.544

Cited by 58 publications

(30 citation statements)

References 8 publications

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“…(5). The change from the ridgelike to a microvillous surface was consistently observed in toad bladders exposed to vasopressin in the presence of an osmotic gradient, a condition which allows the hydro-osmotic response to be elicited.…”

Section: Discussionmentioning

confidence: 80%

“…Notice that the granular cells show almost complete loss of ridges. There is also no apparent luminal swelling of the granular cells, x 2,016. the granular cell of the toad urinary bladder was proposed that the ridges may be a reserve of first described by Davis et al (5). Microridges surface m e m b r a n e to be utilized during stretching.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, a series of investigations employing the scanning electron microscope (SEM) have described the mucosal surface morphology of the toad urinary bladder (4) and the appearance of this surface after the bladder has been exposed to vasopressin (5,25). When toad bladders were stimulated by vasopressin in the presence of an osmotic gradient from the mucosal to serosal solutions, there was a marked change in the mucosal surface morphology of the granular cell.…”

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confidence: 99%

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Mucosal surface morphology of the toad urinary bladder. Scanning electron microscope study of the natriferic and hydro-osmotic response to vasopressin

Mills¹,

Malick²

1978

The Journal of Cell Biology

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The mucosal cell surface of the toad urinary bladder was examined by scanning electron microscopy, and changes in the structure of the surface of the granular cell were correlated with specific physiological responses to vasopressin. Survey views of the mucosal surface demonstrated that there was no consistent repeating anatomical relationship between the granular cell and the mitochondria-rich cell that would support the concept of cooperativeness in the response to vasopressin. During base-line states of Na+-transport and water flux, the microvilli on the mucosal surface of the granular cell are arranged in a ridge-like network with occasional individual projections. When water flux is increased by exposing the tissue to vasopressin, in the presence of an osmotic gradient across the tissue, the microvilli on the granular cell lose the ridge structure and appear, predominantly, as individual projections. Variability-of this appearance points out the necessity of examining large areas and many samples before the significance of any morphological change can be assessed. Blocking the simultaneously occurring natriferic response of the toad urinary bladder with 10 -2 M ouabain does not prevent these changes in the microvilli. When the hydro-osmotic response is blocked by eliminating the osmotic gradient, the granular cell shows no consistent change in mucosal surface morphology even when fixed at the height of the natriferic response. The mitochondria-rich and mucous cells did not show any change in morphology throughout these studies. We conclude that the changes in the mucosal surface morphology of the toad bladder seen after exposure to vasopressin are a result of the increased water flux that occurs when an osmotic gradient exists across the tissue, and are not related to the natdferic response or any specific alteration in the membrane properties. KEY WORDS toad urinary bladder scanningThe toad urinary bladder has long been used as a electron microscopy vasopressin -granular cell model system for studying the action of the poly- 598J. CELL BIOLOGY 9 The Rockefeller University Press 9

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Section: Discussionmentioning

confidence: 80%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Mucosal surface morphology of the toad urinary bladder. Scanning electron microscope study of the natriferic and hydro-osmotic response to vasopressin

Mills¹,

Malick²

1978

The Journal of Cell Biology

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“…It seems unlikely that all the hormonally induced changes in transepithelial transport occur through the MR cell because (1) the area of this flask-shaped cell exposed to the urine is so small that the tissue resistance should be too great to accommodate the observed fluxes, and (2) ELUTION VOLUME (ml) 5 during vasopressin-stimulated hydroosmotic flux (17). On the other hand, our evidence that the MR cell is the site of action of both neurohypophyseal and steroid hormones, together with the recent description of the stellate arrangement of G cells around each MR cell (18), suggests the possibility that the MR cells recognize and amplify the hormonal stimuli and, by some device of intercellular cooperation, regulate the transport activity of the more numerous G cells. The recent observations that cyclic AMP causes a considerable increase in the permeability of epithelial membranes to ions (19) and various metabolites, including nucleotides, may be exchanged between contiguous cells (21)), indicate that cyclic AMP may have a role in intercellular communication in this epithelium.…”

Section: Discussionmentioning

confidence: 81%

Identification of aldosterone-induced proteins in the toad's urinary bladder.

Scott¹,

Sapirstein²

1975

Proc. Natl. Acad. Sci. U.S.A.

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Aldosterone (the 8,11-hemiacetal of 11ft,21-dihydroxy-3,20-dioxo64pregnen-18-sal) markedly stimulates sodium transport in a number of epithelial tissues.-We have attempted to determine whether aldosterone induces the synthesis of specific protein(s) in the course of its action upon the toad urinary bladder. Paired hemibladders were incu ated in' media containing either [3Hlmethionine or [t5S]methionine; aldosterone in physiologic concentrations was added to one bath and, after incubation, the intact "mitochondriarich"' (MR) and "granular" (G) mucosal'cells were isolated. The ratio (3HIIS) was used to identify proteins whose synthesis was induced in the mucosal cells of the steroid-treated bladders. Using exclusion gel chromatography and isoelectric focusing, we identified several aldosterone-induced proteins in the supernatant (105,000 X g) fraction of the MR cell. None was evident in this fraction of the G cell. These proteins have apparent molecular weights ranging from 17,000 to 38,000 and the isoelectric point of the major component is 4.5. Corticosterone (113,21-dihydroxy-4-pregnene-3,20-dione) induced'the synthesis of proteins in the G cells, but none of these proteins was similar in molecularweight to the aldosterone-induced-proteins in the MR cell. Our findings support the hypothesis that aldosterone induces the synthesis of specific proteins and indicate that, in this tissue, these' proteins are synthesized by the MR cell.Aldosterone (the 18,11-hemiacetal of 11f3,21-dihydroxy-3,20-dioxo-4-pregnen-18-al) stimulates the active transport of sodium by the kidney tubule and the toad's urinary bladder (1), a tissue widely used as a model for the distal portion of the mammalian kidney tubule. The biochemical processes leading to this physiologically important effect are in dispute. Suggested mechanisms include (1) enhancement of the apical membrane permeability to sodium, (2) stimulation of the sodium "pump" on the basal membrane of the mucosal cell, and (3) an increase in the metabolic processes energizing sodium transport (2). Because inhibitors of protein and RNA synthesis block the hormonal stimulation of sodium transport, it has been suggested that aldosterone induces the synthesis of proteins directly related to the sodium transport (3). Isolation and characterization of the' steroid-induced proteins, if they exist, should resolve the basic mechanism of aldosterone's effects upon transport.Using a technique for separating the two major morphologic cell types present in the epithelium of the toad bladder (4), we found that the specific binding of aldosterone is lim-. ited to the "mitochondria-rich" (MR) epithelial cell (5). Lo

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“…Thus, micropuncture studies identifying the action of ADH to stimulate sodium transport as a change in resistance of the apical membranes of the mucosal epithelial cells must necessarily be recording effects in the granular cells (20). Similarly there is evidence that ADH stimulates osmotic water flow only in the granular cells (21)(22)(23). If, therefore, the ADH stimulation of osmotic water flow and sodium transport takes place in one cell type, then two compartments of cyclic AMP must also be within these cells.…”

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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Vasopressin-Induced Changes in the Toad Urinary Bladder Epithelial Surface

Cited by 58 publications

References 8 publications

Mucosal surface morphology of the toad urinary bladder. Scanning electron microscope study of the natriferic and hydro-osmotic response to vasopressin

Mucosal surface morphology of the toad urinary bladder. Scanning electron microscope study of the natriferic and hydro-osmotic response to vasopressin

Identification of aldosterone-induced proteins in the toad's urinary bladder.

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

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