scholarly journals The Mechanism of Isotonic Water Transport

1964 ◽  
Vol 48 (1) ◽  
pp. 15-42 ◽  
Author(s):  
Jared M. Diamond
Keyword(s):  
Cell Membrane ◽  
Gall Bladder ◽  
Water Transport ◽  
Water Flow ◽  
Bathing Solution ◽  
Osmotic Gradient ◽  
High Concentration ◽  
Nacl Transport ◽  
Streaming Potentials ◽  
Local Osmosis

The mechanism by which active solute transport causes water transport in isotonic proportions across epithelial membranes has been investigated. The principle of the experiments was to measure the osmolarity of the transported fluid when the osmolarity of the bathing solution was varied over an eightfold range by varying the NaCl concentration or by adding impermeant non-electrolytes. An in vitro preparation of rabbit gall bladder was suspended in moist oxygen without an outer bathing solution, and the pure transported fluid was collected as it dripped off the serosal surface. Under all conditions the transported fluid was found to approximate an NaCl solution isotonic to whatever bathing solution used. This finding means that the mechanism of isotonic water transport in the gall bladder is neither the double membrane effect nor co-diffusion but rather local osmosis. In other words, active NaCl transport maintains a locally high concentration of solute in some restricted space in the vicinity of the cell membrane, and water follows NaCl in response to this local osmotic gradient. An equation has been derived enabling one to calculate whether the passive water permeability of an organ is high enough to account for complete osmotic equilibration of actively transported solute. By application of this equation, water transport associated with active NaCl transport in the gall bladder cannot go through the channels for water flow under passive conditions, since these channels are grossly too impermeable. Furthermore, solute-linked water transport fails to produce the streaming potentials expected for water flow through these passive channels. Hence solute-linked water transport does not occur in the passive channels but instead involves special structures in the cell membrane, which remain to be identified.

scholarly journals Permeability of the Duodenum of the Toad to Non-Electrolytes

1972 ◽  
Vol 25 (5) ◽  
pp. 931 ◽  
Author(s):  
DKC Tay ◽  
GP Findlay
Keyword(s):  
Gall Bladder ◽  
Water Flow ◽  
Streaming Potential ◽  
Reflection Coefficients ◽  
Osmotic Gradient

The reflection coefficients (0") for the permeation, from serosa to mucosa, of 59 different non-electrolytes through the duodenum of the toad have been measured by the method used by Diamond and Wright (1969a) with the rabbit gall bladder. In this method 0" for the solute is the ratio of the streaming potential across the epithelium, resulting from a water flow caused by an osmotic gradient of the test solute, to the streaming potential caused by water flow resulting from an equal osmotic gradient of impermeant solute.

Parathyroid hormone inhibits water flow in the isolated toad bladder

1986 ◽  
Vol 250 (3) ◽  
pp. F532-F538
Author(s):  
S. Sabatini
Keyword(s):  
Parathyroid Hormone ◽  
Epithelial Cells ◽  
Cyclic Amp ◽  
Water Transport ◽  
Water Flow ◽  
Toad Bladder ◽  
High Concentration ◽  
Prostaglandin Release ◽  
Wide Range ◽  
Prostaglandin Inhibitors

These experiments studied the effect of parathyroid hormone (PTH) (1-84) on water and Ca transport in isolated toad bladder sacs and toad bladder epithelial cells. Serosal addition of PTH significantly inhibited maximal water flow induced by vasopressin or exogenous cyclic AMP. This effect was seen over a wide range of concentrations, with the threshold for the effect occurring at 1 ng/ml. Pretreatment of the toad bladder sacs with prostaglandin inhibitors (indomethacin or ibuprofen, 1 X 10(-6) M) or preincubation in low-Ca medium (0.089 mM) abolished the effect of PTH on vasopressin-stimulated water flow. Pretreatment of the toad bladders with lanthanum (5 X 10(-5) M) also abolished the effect of PTH on vasopressin-stimulated water flow. Synthetic PTH (1-34) inhibited vasopressin-stimulated water flow only at a high concentration (1 microgram/ml). PTH increased 45Ca uptake by toad bladder epithelial cells but had no effect on 45Ca efflux. These results demonstrate that PTH inhibits water transport beyond the generation of cyclic AMP. That the effect of PTH was abolished in a low-Ca medium or by pretreatment with lanthanum suggests that cell Ca uptake is required for the effect of PTH on water transport. That prostaglandin inhibitors also block the effect of PTH on vasopressin-stimulated water flow suggests that prostaglandin synthesis is required for the effect. These data suggest that the effect of PTH on water flow is mediated by an increased cellular uptake of Ca that stimulates prostaglandin release. Prostaglandin release, in turn, appears to mediate the inhibitory effect of PTH on vasopressin-stimulated water transport.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Pseudo-streaming potentials in Necturus gallbladder epithelium. II. The mechanism is a junctional diffusion potential.

1992 ◽  
Vol 99 (3) ◽  
pp. 317-338 ◽  
Author(s):  
L Reuss ◽  
B Simon ◽  
C U Cotton
Keyword(s):  
Time Course ◽  
Bathing Solution ◽  
Intercellular Spaces ◽  
Similar Time ◽  
Streaming Potentials ◽  
Osmotic Water ◽  
Lateral Intercellular Spaces ◽  
Transepithelial Voltage ◽  
Time Courses ◽  
Good Agreement

The mechanisms of apparent streaming potentials elicited across Necturus gallbladder epithelium by addition or removal of sucrose from the apical bathing solution were studied by assessing the time courses of: (a) the change in transepithelial voltage (Vms). (b) the change in osmolality at the cell surface (estimated with a tetrabutylammonium [TBA+]-selective microelectrode, using TBA+ as a tracer for sucrose), and (c) the change in cell impermeant solute concentration ([TMA+]i, measured with an intracellular double-barrel TMA(+)-selective microelectrode after loading the cells with TMA+ by transient permeabilization with nystatin). For both sucrose addition and removal, the time courses of Vms were the same as the time courses of the voltage signals produced by [TMA+]i, while the time courses of the voltage signals produced by [TBA+]o were much faster. These results suggest that the apparent streaming potentials are caused by changes of [NaCl] in the lateral intercellular spaces, whose time course reflects the changes in cell water volume (and osmolality) elicited by the alterations in apical solution osmolality. Changes in cell osmolality are slow relative to those of the apical solution osmolality, whereas lateral space osmolality follows cell osmolality rapidly, due to the large surface area of lateral membranes and the small volume of the spaces. Analysis of a simple mathematical model of the epithelium yields an apical membrane Lp in good agreement with previous measurements and suggests that elevations of the apical solution osmolality elicit rapid reductions in junctional ionic selectivity, also in good agreement with experimental determinations. Elevations in apical solution [NaCl] cause biphasic transepithelial voltage changes: a rapid negative Vms change of similar time course to that of a Na+/TBA+ bi-ionic potential and a slow positive Vms change of similar time course to that of the sucrose-induced apparent streaming potential. We conclude that the Vms changes elicited by addition of impermeant solute to the apical bathing solution are pseudo-streaming potentials, i.e., junctional diffusion potentials caused by salt concentration changes in the lateral intercellular spaces secondary to osmotic water flow from the cells to the apical bathing solution and from the lateral intercellular spaces to the cells. Our results do not support the notion of junctional solute-solvent coupling during transepithelial osmotic water flow.

Cellular membrane-anchored fluorescent probe with aggregation-induced emission characteristics for selective detection of Cu2+ ions

2017 ◽  
Vol 196 ◽  
pp. 377-393 ◽  
Author(s):  
Danni Liu ◽  
Shenglu Ji ◽  
Heran Li ◽  
Liang Hong ◽  
Deling Kong ◽  
...  
Keyword(s):  
Aqueous Solution ◽  
Cell Membrane ◽  
Water Solubility ◽  
Live Cells ◽  
Probe Design ◽  
Specific Cell ◽  
Selective Detection ◽  
High Concentration ◽  
Aggregation Induced Emission ◽  
Emissive Probes

The exploration of advanced fluorescent probes that can detect divalent copper (Cu2+) in aqueous environments and even in live organisms is particularly valuable for understanding the occurrence and development of Cu2+-related diseases. In this work, we report the design and synthesis of an aggregation-induced emission luminogen (AIEgen)-based probe (TPE-Py-EEGTIGYG) by integrating an AIEgen, TPE-Py, with a peptide, EEGTIGYG, which can selectively detect Cu2+ in both aqueous solution and live cells. Peptide EEGTIGYG has dual functionality in the probe design, namely improving water solubility and providing specific cell membrane-binding ability. TPE-Py-EEGTIGYG can self-assemble into nanoaggregates at high concentration in aqueous solution (e.g., 25 μM), which possess large fluorescence output due to the restriction of intramolecular rotation of the phenyl rings on TPE-Py. The fluorescence of the TPE-Py-EEGTIGYG nanoaggregates can be significantly quenched by Cu2+ but not by other metal ions, achieving the selective detection of Cu2+ in aqueous media. Furthermore, TPE-Py-EEGTIGYG can exist as a molecular species and is very weakly fluorescent in dilute aqueous solution (e.g., 5 μM), but can however largely switch on its fluorescence upon specifically anchoring onto the cell membrane. The emissive probes on the cell membrane can be used for the detection of Cu2+ ions that move in and out of cells with a fluorescence “turn-off” mode.

An electrical method of measuring non-electrolyte permeability

1969 ◽  
Vol 172 (1028) ◽  
pp. 203-225 ◽  
Keyword(s):  
Gall Bladder ◽  
Streaming Potential ◽  
Concentration Gradients ◽  
Bladder Epithelium ◽  
Electrical Method ◽  
Streaming Potentials ◽  
Unstirred Layers ◽  
Large Numbers ◽  
Tracer Methods

A rapid procedure based on that of Smyth & Wright (1966) is described for obtaining a measure of the permeability of rabbit gall-bladder epithelium to non-electrolytes. The underlying principles are that concentration gradients of permeant molecules produce lower rates of osmotic flow across a membrane than does the same gradient of an impermeant molecule, and that streaming potentials in the gall-bladder are directly proportional to the flow rate. Hence reflexion coefficients (cr’s) were calculated as the ratio of the streaming potential produced by a 0* 1 m gradient of the test solute to the streaming potential produced by a 0T m gradient of an impermeant reference solute, sucrose. The method yields results in agreement with those obtained in the gall-bladder by a zero-flow procedure. In general, the patterns of permeation derived are similar to those obtained in other tissues by the same procedure, by other osmotic procedures, or by direct chemical or tracer methods. The advantages of the method are that (a) large numbers of cr’s can be determined in one experiment with an average standard deviation of ± 8 % ; and (b) the minimum elapsed time between the preparation of a solution and the determination of or is about 90 s, so that cr’s may be obtained for some non-electrolytes subject to gradual chemical transformation in aqueous solution, such as aldehydes. The principles underlying osmotic methods of measuring permeability, and the effects of unstirred layers, are discussed.

Effects of Drugs on Mucus Glycoproteins and Water in Bronchial Secretion

1979 ◽  
Vol 7 (5) ◽  
pp. 434-442 ◽  
Author(s):  
T C Medici ◽  
P Radielovic
Keyword(s):  
Water Content ◽  
Water Transport ◽  
Animal Experiments ◽  
Osmotic Gradient ◽  
Bronchial Mucosa ◽  
Bronchial Secretion ◽  
Epithelial Surface ◽  
Bronchial Mucus ◽  
Mucus Glycoproteins

The result of chemical analysis of the bronchial secretion is simple; up to 95% of the secretion is made up of water, and up to 5% is composed of ash, protein, carbohydrate, lipid, nitrogen and desoxyribonucleic acid. More complicated is the question of how bronchial secretion is formed and of which active biological components it is composed. Bronchial secretion is the result of the different processes, secretion, transudation, exudation and exfoliation from a highly differentiated bronchial mucosa. To those substances secreted belong, amongst others, constituents important for the flow properties and the transportability of the secretion: the bronchial mucus glycoproteins and water. The bronchial glycoproteins are the most important group, constituting 50–80% of the macromolecules. They are formed and secreted by the bronchial mucosa. The synthesis and secretion of bronchial glycoproteins are influenced by drugs in different ways. Beta-adrenergic stimulants do not alter these processes in in vitro studies on human glands, although an increase in mucus of glycoprotein production has been demonstrated in animal experiments and indirectly in man. Cyclic adenosine monophosphate and the methylxanthines stimulate mucus glycoprotein production, anticholinergic agents reduce but do not completely supress this process. Anti-allergic agents do not alter the production of bronchial glycoproteins with the exception of the corticosteroids which partially inhibit the synthesis and secretion. Neither expectorants nor mucolytic agents influence the production of mucus glycoproteins in human bronchial glands as opposed to animal experiments, in which these compounds produce an increase in the output of the bronchial fluid. Water constitutes 95% of the bronchial secretion and the water content considerably influences mucociliary function. An osmotic gradient, the result of active sodium and chloride ion transport across the bronchial epithelium, ensures on the one hand that water diffuses through epithelium on to the epithelial surface where it forms the serous sol layer in which the cilia beat. On the other hand water is probably transported in the same way across the mucosal glands where it mixes with the extremely hydrophilic mucus glycoproteins. The ion and water transport is influenced by drugs. Acetylcholine, histamine and terbutaline stimulate the ion and thereby water transport. Atropine, diphenylhydramine, an H1-antagonist, propranolol, a beta-blocker andfurosemide inhibit these transport mechanisms. Whether ketotifen, a new antihistaminic drug used in the treatment of bronchial asthma, will affect these processes, decreasing the water content of bronchial mucus, remains to be seen.

Antidiuretic hormone-dependent membrane capacitance and water permeability in the toad urinary bladder

1983 ◽  
Vol 244 (2) ◽  
pp. F195-F204
Author(s):  
L. G. Palmer ◽  
M. Lorenzen
Keyword(s):  
Antidiuretic Hormone ◽  
Water Flow ◽  
Time Course ◽  
Apical Membrane ◽  
Constant Current ◽  
Apical Plasma Membrane ◽  
Voltage Response ◽  
Toad Urinary Bladder ◽  
Osmotic Gradient ◽  
Capacitance Change

Antidiuretic hormone (ADH) increased the electrical capacitance of apical membrane of the toad bladder; this effect was modulated by the osmotic gradient across the tissue. Capacitance was measured from the transepithelial voltage response to constant-current pulses using bladders depolarized with KCl-sucrose serosal solution to reduce basolateral resistance and with Na-free mucosal solution to increase apical membrane resistance. Addition of ADH (20 mU/ml) increased capacitance by 28 +/- 9% (mean +/- SD) in the absence and by 8 +/- 3% in the presence of an osmotic gradient (200 mosM, mucosal side hypotonic). With bladders stimulated in the absence of an osmotic gradient, rapidly imposing a gradient resulted in a peak rate of water flow that declined to 40% of the peak value after 15-20 min. ADH-dependent capacitance also decreased with a similar time course. Removal of ADH reversed the capacitance change (t1/2 = 10-15 min), but the reversal was slower than the decline in water flow to basal levels (t1/2 less than 5 min). Colchicine and cytochalasin B also inhibited the ADH-induced capacitance increase. The capacitance change was also inhibited when the mucosal solution was made hypertonic with raffinose. The results are interpreted within the framework of a previously proposed model of ADH-stimulated water transport in which cytoplasmic vesicular structures fuse with the apical plasma membrane.

In vivo inhibition of transcellular water channels (aquaporin-1) during acute peritoneal dialysis in rats

1996 ◽  
Vol 271 (6) ◽  
pp. H2254-H2262 ◽  
Author(s):  
O. Carlsson ◽  
S. Nielsen ◽  
el-R. Zakaria ◽  
B. Rippe
Keyword(s):  
Peritoneal Dialysis ◽  
Water Transport ◽  
Water Flow ◽  
Peritoneal Cavity ◽  
Critical Role ◽  
Water Channels ◽  
Capillary Endothelium ◽  
Tissue Fixation ◽  
Solute Permeability ◽  
Aquaporin 1

During peritoneal dialysis (PD), a major portion of the osmotically induced water transport to the peritoneum can be predicted to occur through endothelial water-selective channels. Aquaporin-1 (AQP-1) has recently been recognized as the molecular correlate to such channels. Aquaporins can be inhibited by mercurials. In the present study, HgCl2 was applied locally to the peritoneal cavity in rats after short-term tissue fixation, used to protect the tissues from HgCl2 damage. Dianeal (3.86%) was employed as dialysis fluid, 125I-albumin as an intraperitoneal volume marker, and 51Cr-EDTA (constantly infused intravenously) to assess peritoneal small-solute permeability characteristics. Immunocytochemistry and immunoelectron microscopy revealed abundant AQP-1 labeling in capillary endothelium in peritoneal tissues, representing sites for HgCl2 inhibition of water transport. HgCl2 treatment reduced water flow and inhibited the sieving of Na+ without causing any untoward changes in microvascular permeability, compared with that of fixed control rats, in which the peritoneal cavity was exposed to tissue fixation alone. In fixed control rats, the mean intraperitoneal volume (IPV) increased from 20.5 +/- 0.15 to 25.0 +/- 0.52 ml in 60 min, whereas in the HgCl2-treated rats, the increment was only from 20.7 +/- 0.23 to 23.5 +/- 0.4 ml. In fixed control rats, the dialysate Na+ fell from 135.3 +/- 0.97 to 131.3 +/- 1.72 mM, whereas in the HgCl2-treated rats the dialysate Na+ concentration remained unchanged between 0 and 40 min, further supporting that water channels had been blocked. Computer simulations of peritoneal transport were compatible with a 66% inhibition of water flow through aquaporins. The observed HgCl2 inhibition of transcellular water channels strongly indicates a critical role of aquaporins in PD and provides evidence that water channels are crucial in transendothelial water transport when driven by crystalloid osmosis.

Water flow inside various geometric nano-confinement channels

2020 ◽  
Vol 22 (42) ◽  
pp. 24633-24639
Author(s):  
Xujun Xu ◽  
Yanyan Zhao ◽  
Jicheng Wang ◽  
Ning Zhang ◽  
Chunlei Wang ◽  
...  
Keyword(s):  
Water Transport ◽  
Water Flow ◽  
Confined Systems

In nano-confined systems, the properties of a fluid are different from those of macroscopic systems, and the properties of a nanotube can significantly affect water transport.

scholarly journals Production of normal mice from spermatozoa denatured with high alkali treatment before ICSI

Reproduction ◽  
2009 ◽  
Vol 137 (5) ◽  
pp. 779-792 ◽  
Author(s):  
Chong Li ◽  
Eiji Mizutani ◽  
Tetsuo Ono ◽  
Teruhiko Wakayama
Keyword(s):  
Cell Membrane ◽  
Alkali Treatment ◽  
Methylation Status ◽  
Control Group ◽  
Oocyte Activation ◽  
Dna Double Strand Breaks ◽  
High Concentration ◽  
Developmental Potential ◽  
Normal Offspring ◽  
Activation Capacity

In mammals, ICSI is now a very important tool for both assisted reproductive technology and studying the mechanisms of fertilization. In the latter experiments, it is important to use spermatozoa that have lost their oocyte activation capacity but still retain their developmental potential. In this study, we used high-concentration NaOH to remove oocyte activation potential from spermatozoa, and examined whether normal offspring could be generated from these spermatozoa after ICSI. The spermatozoa were treated with different concentrations of NaOH (1–100 mM) for 1 h and then neutralized with equal amounts of same concentration of HCl. In 10 mM NaOH-treated spermatozoa, the cell membrane was broken and most of them failed to activate oocytes after their injection into the oocytes. However, these spermatozoa did not show strong damage, and after artificial activation with SrCl2, all of the zygotes were judged as normal by immunostaining to check the methylation status of histone H3 lysine 9, low chromosome damage by karyotype assay and staining with DNA double-strand breaks marker, γH2AX. Moreover, after transferring those embryos into recipient females, 106 (36.7%) live and healthy offspring were delivered, which is similar to the rate in the fresh control group. By contrast, spermatozoa treated with lower NaOH concentrations retained their oocyte activation capacity and those treated with higher concentrations lost their developmental potential. This suggests that 10 mM NaOH for 1 h is the best treatment to completely destroy the cell membrane and activation capacity of spermatozoa without injuring their developmental potential.

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