scholarly journals Water transport and homeostasis as a major function of erythrocytes

2018 ◽  
Vol 314 (5) ◽  
pp. H1098-H1107 ◽  
Author(s):  
Joseph Sugie ◽  
Marcos Intaglietta ◽  
Lanping Amy Sung

Erythrocytes have long been known to change volumes and shapes in response to different salt concentrations. Aquaporin-1 (AQP1) was discovered in their membranes more than 20 yr ago. The physiological roles of volume changes and AQP1 expression, however, have remained unclear. We propose that rapid water exchange through AQP1 coupled with large capacity for volume change may allow erythrocytes to play an important role in water regulation. In this study, we showed that erythrocytes in situ gradually reduced their volumes by 39% in response to the hyperosmotic corticomedullary gradient within mouse kidneys. AQP1 knockout (KO) erythrocytes, however, displayed only minimal reduction. Constructing a microfluidic device resembling capillary flow with an extracellular fluorescent reporter demonstrated that water exchanges between erythrocytes and their hypotonic or hypertonic surroundings in vitro reached steady state in ~60 ms. AQP1 KO erythrocytes, however, did not show significant change. To simulate the water transport in circulation, we built basic units consisting of three compartments (i.e., erythrocyte, plasma, and interstitial fluid) using Kedem-Katchalsky equations for membrane transport, and connected multiple units to account for the blood flow. These simulations agreed with experimental results. Importantly, volume-changing erythrocytes in capillaries always “increase” the osmotic gradient between plasma and interstitial fluid, making them function as “micropumps” to speed up the regulation of local osmolarity. Trillions of these micropumps, mobile throughout the body, may further contribute to water homeostasis. These insights suggest that the enhanced exchange of water, in addition to O2 and CO2, may well be the third major function of erythrocytes. NEW & NOTEWORTHY Physiological roles of erythrocyte volume change and aquaporin-1 were proposed and investigated here. We conclude that fast water transport by aquaporin-1 coupled with large volume-change capacity allows erythrocytes to enhance water exchange with local tissues. Furthermore, their huge number and mobility allow them to contribute to body water homeostasis.

1999 ◽  
Vol 276 (1) ◽  
pp. C76-C81 ◽  
Author(s):  
Baoxue Yang ◽  
Hans G. Folkesson ◽  
Jian Yang ◽  
Michael A. Matthay ◽  
Tonghui Ma ◽  
...  

Aquaporin-1 (AQP1) water channels are expressed widely in epithelia and capillary endothelia involved in fluid transport. To test whether AQP1 facilitates water movement from capillaries into the peritoneal cavity, osmotically induced water transport rates were compared in AQP1 knockout [(−/−)], heterozygous [(+/−)], and wild-type [(+/+)] mice. In (+/+) mice, RT-PCR showed detectable transcripts for AQP1, AQP3, AQP4, AQP7, and AQP8. Immunofluorescence showed AQP1 protein in capillary endothelia and mesangium near the peritoneal surface and AQP4 in adherent muscle plasmalemma. For measurement of water transport, 2 ml of saline containing 300 mM sucrose (600 mosM) were infused rapidly into the peritoneal cavity via a catheter. Serial fluid samples (50 μl) were withdrawn over 60 min, with albumin as a volume marker. The albumin dilution data showed significantly decreased initial volume influx in AQP1 (−/−) mice: 101 ± 8, 107 ± 5, and 42 ± 4 (SE) μl/min in (+/+), (+/−), and (−/−) mice, respectively [ n = 6–10, P < 0.001, (−/−) vs. others]. Volume influx for AQP4 knockout mice was 100 ± 8 μl/min. In the absence of an osmotic gradient,3H2O uptake [half time = 2.3 and 2.2 min in (+/+) and (−/−) mice, respectively], [14C]urea uptake [half time = 7.9 and 7.7 min in (+/+) and (−/−) mice, respectively], and spontaneous isosmolar fluid absorption from the peritoneal cavity [0.47 ± 0.05 and 0.46 ± 0.04 ml/h in (+/+) and (−/−) mice, respectively] were not affected by AQP1 deletion. Therefore, AQP1 provides a major route for osmotically driven water transport across the peritoneal barrier in peritoneal dialysis.


2010 ◽  
Vol 30 (2) ◽  
pp. 135-141 ◽  
Author(s):  
Olivier Devuyst ◽  
Andrea J. Yool

Peritoneal dialysis involves diffusive and convective transport and osmosis through the highly vascularized peritoneal membrane. Several lines of evidence have demonstrated that the water channel aquaporin-1 (AQP1) corresponds to the ultrasmall pore predicted by the model of peritoneal transport. Proof-of-principle studies have shown that upregulation of the expression of AQP1 in peritoneal capillaries results in increased water permeability and ultrafiltration, without affecting the osmotic gradient or small solute permeability. Conversely, studies in Aqp1 mice have shown that haplo-insufficiency for AQP1 results in significant attenuation of water transport. Recent studies have demonstrated that AQP1 is involved in the migration of different cell types, including endothelial cells. In parallel, chemical screening has identified lead compounds that could act as antagonists or agonists of AQPs, with description of putative binding sites and potential mechanisms of gating the water channel. By modulating water transport, these pharmacological agents could have clinically relevant effects in targeting specific tissues or disease states.


Water exchange between insects and their environment via the vapour phase includes influx and efflux components. The pressure cycle theory postulates that insects (and some other arthropods) can regulate the relative rates of influx and efflux of water vapour by modulating hydrostatic pressures at a vapour-liquid interface by compressing or expanding a sealed, gas-filled cavity. Some such cavities, like the tracheal system, could be compressed by elevated pressure in all or part of the haemocoele. Others, perhaps including the muscular rectum of flea prepupae, could be compressed by intrinsic muscles. Maddrell Insect Physiol . 8, 199 (1971)) suggested a pressure cycle mechanism of this kind to account for rectal uptake of water vapour in Thermobia but did not find it compatible with quantitative information then available. Newer evidence conforms better with the proposed mechanism. Cyclical pressure changes are of widespread occurrence in insects and have sometimes been shown to depend on water status. Evidence is reviewed for the role of the tracheal system as an avenue for net exchange of water between the insect and its environment. Because water and respiratory gases share common pathways, most published findings fail to distinguish between the conventional view that the tracheal system has evolved as a site for distribution and exchange of respiratory gases and that any water exchange occurring in it is generally incidental and nonadaptive, and the theory proposed here. The pressure cycle theory offers a supplementary explanation not incompatible with evidence so far available. The relative importance of water economy and respiratory exchange in the functioning of compressible cavities such as the tracheal system remains to be explored. Some further implications of the pressure cycle theory are discussed. Consideration is given to the possible involvement of vapour-phase transport in the internal redistribution of water within the body. It is suggested that some insect wings may constitute internal vapour-liquid exchange sites, where water can move from the body fluids to the intratracheal gas. Ambient and body temperature must influence rates of vapour-liquid mass transfer. If elevated body temperature promotes evaporative discharge of the metabolic water burden that has been shown to accumulate during flight in some large insects, their minimum threshold thoracic temperature for sustained flight may relate to the maintenance of water balance. The role of water economy in the early evolution of insect wings is considered. Pressure cycles might help to maintain water balance in surface-breathing insects living in fresh and saline waters, but the turbulence of the surface of the open sea might prevent truly marine forms from using this mechanism.


Author(s):  
Mohsen Askarbioki ◽  
Mojtaba Mortazavi ◽  
Abdolhamid Amooee ◽  
Saeid Kargar ◽  
Mohammad Afkhami-Ardekani ◽  
...  

Objective: Today, there are various non-invasive techniques available for the determination of blood glucose levels. In this study, the level of blood glucose was determined by developing a new device using near-infrared (NIR) wavelength, glass optical waveguide, and the phenomenon of evanescent waves. Materials and Methods: The body's interstitial fluid has made possible the development of new technology to measure the blood glucose. As a result of contacting the fingertip with the body of the borehole rod, where electromagnetic waves are reflected inside, evanescent waves penetrate from the borehole into the skin and are absorbed by the interstitial fluid. The electromagnetic wave rate absorption at the end of the borehole rod is investigated using a detection photodetector, and its relationship to the people's actual blood glucose level. Following precise optimization and design of the glucose monitoring device, a statistical population of 100 participants with a maximum blood glucose concentration of 200 mg/dL was chosen. Before measurements, participants put their index finger for 30 seconds on the device. Results: According to this experimental study, the values measured by the innovative device with Clark grid analysis were clinically acceptable in scales A and B. The Adjusted Coefficient of Determination of the data was estimated to be 0.9064. Conclusion: For future investigations, researchers are recommended to work with a larger statistical population and use error reduction trends to improve the accuracy and expand the range of measurements.


Neurology ◽  
2018 ◽  
Vol 91 (11) ◽  
pp. 515-522 ◽  
Author(s):  
Stéphanie Lenck ◽  
Ivan Radovanovic ◽  
Patrick Nicholson ◽  
Mojgan Hodaie ◽  
Timo Krings ◽  
...  

The recent discoveries of the glymphatic and lymphatic systems of the brain have helped advance our understanding of CSF physiology and may allow new insights in the understanding of idiopathic intracranial hypertension (IIH). The clinical and radiologic presentations of IIH appear to be related to congestion of the glymphatic system associated with an overflow of the lymphatic CSF outflow pathway. By revisiting the role of “vascular arachnoid granulations” in the brain, we hypothesize that an initial impairment of the transport of interstitial fluid from the glymphatic system to the venous blood of the dural sinuses may trigger the hydrodynamic cascade of IIH. Furthermore, we speculate that, similar to other water-exchange systems in the brain, a specific subtype of aquaporin is involved in this transport. This theory may eventually help to provide an underlying explanation for IIH and its associated conditions, since in most of them, the expression of several aquaporins is altered.


1979 ◽  
Vol 7 (5) ◽  
pp. 434-442 ◽  
Author(s):  
T C Medici ◽  
P Radielovic

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.


1937 ◽  
Vol 33 (2) ◽  
pp. 132-142
Author(s):  
A. I. Golikov ◽  
M. M. Grigorieva

The study of the problem of water exchange and issues of the pathogenesis of edema (Starling, Krog, Beilis, Schade, Gover, Shabanier, Kilin, etc.) made it possible to establish the colossal significance in the pathogenesis of nephrosis of a number of factors associated with the state of the body's proteins. To one degree or another, depletion of blood plasma proteins, sharp changes in the ratio of protein fractions with a shift towards the coarse-dispersed phase (globulins), an increase in the hydrophilicity of tissue colloids (McClure and Aldrich test) characterize pathological shifts in the protein economy of the body. The osmotic pressure of nephrotic plasma proteins drops sharply due to an increase in osmotically much less active globulins and fibrinogen (Schade, Shabanier, Gover, Kilin, Malkin, etc.). This decrease can in some cases reach a value of 10-14 cm of water column in comparison with the normal value of 30-40 cm (Gover, Golikov). According to modern views, these violations of the protein constant due to changes in the salt balance, in the state of permeability of the capillary wall and the state of tissue colloids are a common cause of the hydropic state of the body. Along with the violation of protein metabolism, changes in the state of lipoid-cholesterol metabolism occur in the body with nephrosis. The absence of contraindications for giving nephrotic protein is well known.


Author(s):  
Yoshinori Marunaka

Type 2 diabetes mellitus (T2DM) is one of the most common lifestyle-related diseases (metabolic disorders) due to hyperphagia and/or hypokinesia. Hyperglycemia is the most well-known symptom occurring in T2DM patients. Insulin resistance is also one of the most important symptoms, however, it is still unclear how insulin resistance develops in T2DM. Detailed understanding of the pathogenesis primarily causing insulin resistance is essential for developing new therapies for T2DM. Insulin receptors are located at the plasma membrane of the insulin-targeted cells such as myocytes, adipocytes, etc., and insulin binds to the extracellular site of its receptor facing the interstitial fluid. Thus, changes in interstitial fluid microenvironments, specially pH, affect the insulin-binding affinity to its receptor. The most well-known clinical condition regarding pH is systemic acidosis (arterial blood pH &lt; 7.35) frequently observed in severe T2DM associated with insulin resistance. Because the insulin-binding site of its receptor faces the interstitial fluid, we should recognize the interstitial fluid pH value, one of the most important factors influencing the insulin-binding affinity. It is notable that the interstitial fluid pH is unstable compared with the arterial blood pH even under conditions that the arterial blood pH stays within the normal range, 7.35–7.45. This review article introduces molecular mechanisms on unstable interstitial fluid pH value influencing the insulin action via changes in insulin-binding affinity and ameliorating actions of weak organic acids on insulin resistance via their characteristics as bases after absorption into the body even with sour taste at the tongue.


1996 ◽  
Vol 271 (6) ◽  
pp. H2254-H2262 ◽  
Author(s):  
O. Carlsson ◽  
S. Nielsen ◽  
el-R. Zakaria ◽  
B. Rippe

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.


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