Metabolic evidence that serosal sodium does not recycle through the active transepithelial transport pathway of toad bladder

1976 ◽  
Vol 30 (1) ◽  
pp. 65-77 ◽  
Author(s):  
Mitzy Canessa ◽  
Pedro Labarca ◽  
Alexander Leaf
Keyword(s):  
Toad Bladder ◽  
Transepithelial Transport ◽  
Transport Pathway

scholarly journals Regulation of the sodium permeability of the luminal border of toad bladder by intracellular sodium and calcium: role of sodium-calcium exchange in the basolateral membrane.

1981 ◽  
Vol 77 (6) ◽  
pp. 693-712 ◽  
Author(s):  
H S Chase ◽  
Q Al-Awqati
Keyword(s):  
Calcium Transport ◽  
Basolateral Membrane ◽  
Intracellular Sodium ◽  
Toad Bladder ◽  
Transepithelial Transport ◽  
Sodium Permeability ◽  
Cell Calcium ◽  
Luminal Membrane ◽  
Sodium Calcium ◽  
Sodium Gradient

Sodium movement across the luminal membrane of the toad bladder is the rate-limiting step for active transepithelial transport. Recent studies suggest that changes in intracellular sodium regulate the Na permeability of the luminal border, either directly or indirectly via increases in cell calcium induced by the high intracellular sodium. To test these proposals, we measured Na movement across the luminal membrane (th Na influx) and found that it is reduced when intracellular Na is increased by ouabain or by removal of external potassium. Removal of serosal sodium also reduced the influx, suggesting that the Na gradient across the serosal border rather than the cell Na concentration is the critical factor. Because in tissues such as muscle and nerve a steep transmembrane sodium gradient is necessary to maintain low cytosolic calcium, it is possible that a reduction in the sodium gradient in the toad bladder reduces luminal permeability by increasing the cell calcium activity. We found that the inhibition of the influx by ouabain or low serosal Na was prevented, in part, by removal of serosal calcium. To test for the existence of a sodium-calcium exchanger, we studied calcium transport in isolated basolateral membrane vesicles and found that calcium uptake was proportional to the outward directed sodium gradient. Uptake was not the result of a sodium diffusion potential. Calcium efflux from preloaded vesicles was accelerated by an inward directed sodium gradient. Preliminary kinetic analysis showed that the sodium gradient changes the Vmax but not the Km of calcium transport. These results suggest that the effect of intracellular sodium on the luminal sodium permeability is due to changes in intracellular calcium.

Water-permeable and -impermeable barriers of snake distal tubules

1984 ◽  
Vol 246 (3) ◽  
pp. F290-F299 ◽  
Author(s):  
K. W. Beyenbach
Keyword(s):  
Epithelial Cell ◽  
Apical Membrane ◽  
Basolateral Membrane ◽  
Cell Swelling ◽  
Transepithelial Transport ◽  
Pressure Gradients ◽  
Transport Pathway ◽  
Luminal Membrane ◽  
Apical Side ◽  
Distal Tubules

Isolated perfused snake distal tubules transport Na from lumen bath via an amiloride-sensitive transport pathway. Elevation of the luminal Na concentration from 16 to 150 mM leads to non-steady-state electrical behavior and cell swelling. To elucidate the mechanism of cell swelling, the water permeabilities of the epithelium and its apical and basolateral membrane were assessed. Distal tubules were found to be virtually impermeable to transepithelial water flow. Hydraulic conductivity measured 1.2 X 10(-7) cm3 X s-1 X cm-2 X atm-1 in the absence or presence of vasopressin. Effects of transepithelial osmotic pressure gradients on epithelial cell volume revealed the luminal membrane as the water-impermeable cellular barrier and the basolateral membrane as a barrier that is freely permeable to water. Epithelial cell swelling was blocked during perfusion with 150 mM Na when the perfusate also contained amiloride (10(-5) M). These results support the hypothesis that, in the case of transepithelial transport in the presence of high luminal Na concentrations, Na entry across the apical membrane exceeds Na extrusion across the basolateral membrane. Hence, the cells accumulate solute: Na from the apical side and some anion from the apical and/or serosal side. Concomitantly, the epithelial cells swell as water enters across the highly permeable basolateral membrane.

Comments on: Sodium fluxes through the active transport pathway in toad bladder

1975 ◽  
Vol 24 (1) ◽  
pp. 401-406 ◽  
Author(s):  
A. Essig ◽  
M. A. Lang ◽  
M. Walser ◽  
J. S. Chen
Keyword(s):  
Active Transport ◽  
Toad Bladder ◽  
Transport Pathway

scholarly journals Transepithelial transport across the blood–testis barrier

Reproduction ◽  
2018 ◽  
Vol 156 (6) ◽  
pp. R187-R194 ◽  
Author(s):  
Siennah R Miller ◽  
Nathan J Cherrington
Keyword(s):  
Genital Tract ◽  
Drug Disposition ◽  
Nucleoside Analogs ◽  
The Body ◽  
Transepithelial Transport ◽  
Male Genital Tract ◽  
Transport Pathway ◽  
Transport Pathways ◽  
Male Genital ◽  
Blood Testis Barrier

The blood–testis barrier protects developing germ cells by limiting the entry of xenobiotics into the adluminal compartment. There is strong evidence that the male genital tract can serve as a sanctuary site, an area of the body where tumors or viruses are able to survive treatments because most drugs are unable to reach therapeutic concentrations. Recent work has classified the expression and localization of endogenous transporters in the male genital tract as well as the discovery of a transepithelial transport pathway as the molecular mechanism by which nucleoside analogs may be able to circumvent the blood–testis barrier. Designing drug therapies that utilize transepithelial transport pathways may improve drug disposition to this sanctuary site. Strategies that improve disposition into the male genital tract could reduce the rate of testicular relapse, decrease viral load in semen, and improve therapeutic strategies for male fertility.

Sodium fluxes through the active transport pathway in toad bladder

1975 ◽  
Vol 21 (1) ◽  
pp. 87-98 ◽  
Author(s):  
Jing S. Chen ◽  
Mackenzie Walser
Keyword(s):  
Active Transport ◽  
Toad Bladder ◽  
Transport Pathway

Electrolyte transport in kidney tubule cells

1971 ◽  
Vol 262 (842) ◽  
pp. 175-196 ◽  
Keyword(s):  
Potential Gradient ◽  
Transepithelial Transport ◽  
Physical Factors ◽  
Tubule Cell ◽  
K Uptake ◽  
Transport Pathway ◽  
Proximal Tubular ◽  
K Secretion ◽  
Potassium Secretion ◽  
Membrane Changes

Transtubular movement of Na and K takes place across an electrically negative cell compartment rich in K and poor in Na. Some properties of the luminal and peritubular cell boundaries with respect to ionic pump and leak characteristics are analysed. Sodium enters the tubule cell from the lumen down an electrochemical potential gradient. Peritubular Na-extrusion takes place both by an ouabain-sensitive Na-K exchange pump and by an electrogenic ouabain-insensitive Na pump. Net Na transport can be uncoupled from peritubular K uptake. It is highly likely that peritubular K uptake is pH sensitive. Once sodium has been extruded into the peritubular infoldings net Na transepithelial-transport is further critically affected by physical factors regulating capillary uptake of interstitial fluid. Several lines of evidence indicate that a large, variable intercellular transport pathway is present at the proximal tubular level. Tubular K secretion is controlled at the distal tubular level by: (1) the interplay of luminal and peritubular active K uptake into the tubule cell and (2) by a variable passive leak of K from cell into lumen across the partly depolarized luminal cell membrane. Changes in active peritubular K uptake regulate the size of a relatively small intracellular K transport pool and are critically involved in setting the rate of net tubular potassium secretion.

Transepithelial transport and its hormonal control in toad bladder

1965 ◽  
Vol 56 (1) ◽  
pp. 216-263 ◽  
Author(s):  
Alexander Leaf
Keyword(s):  
Hormonal Control ◽  
Toad Bladder ◽  
Transepithelial Transport

Inhibition of urea transport in inner medullary collecting duct by phloretin and urea analogues

1989 ◽  
Vol 257 (3) ◽  
pp. F359-F365 ◽  
Author(s):  
C. L. Chou ◽  
M. A. Knepper
Keyword(s):  
Water Permeability ◽  
Collecting Duct ◽  
Water Channel ◽  
Toad Bladder ◽  
Lipid Phase ◽  
Urea Transport ◽  
Transport Pathway ◽  
Inner Medullary Collecting Duct ◽  
Urea Permeability ◽  
Medullary Collecting Duct

Arginine vasopressin (AVP) increases the urea permeability of the rat terminal inner medullary collecting duct (IMCD) to levels much greater than can be explained by lipid-phase permeation or paracellular diffusion, suggesting the presence of an AVP-stimulated facilitated transport pathway. We tested whether inhibitors of facilitated urea transport in erythrocytes and toad bladder also inhibit urea transport in the isolated perfused IMCD. Apparent urea permeability (Purea) was determined by measuring the flux due to an imposed 5 mM concentration gradient. Phloretin (0.25 mM in lumen or bath) reversibly inhibited Purea. Phloretin, however, did not alter the osmotic water permeability. Urea analogues (200 mM) in the bath inhibited Purea (thiourea, 74% inhibition; methylurea 65%; acetamide 35%). Urea analogues in the lumen decreased Purea with the same order of potency. The inhibitory K1/2 for thiourea in the lumen was 27 +/- 2 mM and did not change with 10(-10) M AVP (28 +/- 3), despite a fourfold increase in Purea. We conclude the following. 1) Inhibitor actions on urea transport in the IMCD are similar to those in red blood cells and toad bladder, suggesting that the urea transporter could be a membrane protein similar to that in the other tissues. 2) Inhibition of Purea by phloretin without an effect on vasopressin-stimulated water permeability supports the view that the urea pathway is not the vasopressin-stimulated water channel. 3) The ability of AVP to increase Purea without an effect on the inhibitory K1/2 for thiourea indicates that AVP probably does not act by altering the binding affinity of individual transporters for urea.

scholarly journals Uptake and transepithelial transport of nerve growth factor in suckling rat ileum.

1986 ◽  
Vol 103 (5) ◽  
pp. 1979-1990 ◽  
Author(s):  
K Siminoski ◽  
P Gonnella ◽  
J Bernanke ◽  
L Owen ◽  
M Neutra ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Transepithelial Transport ◽  
Immunological Methods ◽  
Transport Pathway ◽  
Nerve Growth ◽  
Rat Ileum ◽  
Absorptive Cells

Nerve growth factor (NGF) is necessary for the development of sympathetic and some sensory neurons. Milk may be a source of NGF for suckling young, but sites of intestinal absorption of the protein have not been identified. To determine whether NGF is transported across the absorptive epithelium of suckling rat ileum, we assessed binding, uptake, and transport of 125I-NGF by light microscopy and EM autoradiography. Blood and tissue extracts were analyzed by biochemical and immunological methods to determine whether NGF was taken up structurally intact. NGF binding sites were identified on microvilli and apical invaginations of ileal absorptive cells in vitro. Injected into ileal loops in vivo, NGF radioactivity retained by fixation was evident after 20 min in apical regions of absorptive cells, in endocytic tubules (which mediate the uptake of membrane-bound ligands), in vesicles (which mediate nonspecific endocytosis), and in the supranuclear lysosomal vacuole. At 1 and 2 h, radiolabel in these compartments increased and silver grains were evident at the basal cell surface, and in cells, matrix, and vessels of the lamina propria. In blood and liver, radiolabeled molecules that were immunologically and electrophoretically indistinguishable from NGF and that co-eluted with NGF on gel filtration columns were detected, confirming that some NGF was transported across the epithelium structurally intact. Thus, absorptive cells of suckling rat ileum can take up NGF by both receptor-mediated and nonspecific endocytosis, and direct NGF either to the lysosome for degradation, or into a transepithelial transport pathway.

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