Fluid absorption and active and passive ion flows in the rabbit superficial pars recta

Schafer, James A.; Patlak, C. S.; Andreoli, Thomas E.

doi:10.1152/ajprenal.1977.233.2.f154

Cited by 21 publications

(28 citation statements)

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“…Based on our experimental data and mathematic modeling of the spaces [31][32][33], as well as the previously known high ionic conductance of the proximal tubule, we concluded that the osmolality at the apical ends of the spaces would be well less than 1 mmol/L hyperosmotic to the external solution even under the most extreme conditions. The lack of a significant diffusion resistance in the lateral spaces of the proximal tubule was also supported by examinations of their three-dimensional morphology.…”

Section: Isosmotic Volume Reabsorption By the Proximal Tubulesupporting

confidence: 55%

Renal water reabsorption: A physiologic retrospective in a molecular era

Schafer

2004

Kidney International

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The cloning and sequencing of the aquaporin water channels has been an enormous advance in the biomedical sciences, as recognized by the award of the Nobel Prize to Peter Agre last year. Among many other examples, expression of aquaporin proteins in Xenopus oocytes and other heterologous expression systems has confirmed two important models of renal function: the increase in the water permeability of the collecting duct by antidiuretic hormone (ADH), and the mechanism of near isosmotic volume reabsorption by the proximal tubule. These mechanisms were the subjects of intensive investigation by numerous investigators, including Thomas E. Andreoli, who is being honored by this symposium, and who developed many of the key concepts in these areas. His early work with artificial lipid bilayer membranes and the pore-forming antibiotic amphotericin provided the rigorous foundation in experimental and conceptual modeling techniques that he later applied to physiologic and pathophysiologic mechanisms in the kidney, which are summarized in this retrospective. Dr. Andreoli and his colleagues proposed a water channel mechanism for the action of ADH, which has been confirmed by the cloning and heterologous expression of aquaporin-2. They also proposed that volume reabsorption by the proximal tubule depended on a very high hydraulic conductivity and the development of luminal hypotonicity produced by active solute reabsorption. This model has also been confirmed in mice in which aquaporin-1 expression is knocked out, resulting in a low proximal tubule water permeability that exaggerates the development of luminal hypotonicity.

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Section: Isosmotic Volume Reabsorption By the Proximal Tubulesupporting

confidence: 55%

Renal water reabsorption: A physiologic retrospective in a molecular era

Schafer

2004

Kidney International

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“…Several models and theoretical treatments have been formulated to account for isosmotic fluid absorption in tubular and planar epithelia (Curran and Macintosh, 1962;Diamond and Bossert, 1967;Hill, 1975aHill, , b, 1980Sackin and Boulpaep, 1975;Schafer et al, 1975;Schafer et al, 1977;Hill and Hill, 1978;Diamond, 1979;Weinstein and Stephenson, 1981). Unfortunately, the assumptions and predictions have proved difficult to validate and demonstrate experimentally (see Diamond, 1979;Hill, 1980;Reuss and Cotton, 1988).…”

Section: Discussionmentioning

confidence: 99%

“…Several epithelia, including renal proximal tubule, intestine, and gallbladder, transport salt and water in near isosmotic proportions (Curran and Solomon, 1957;Diamond, 1962Diamond, , 1978Diamond, , 1979Whitlock and Wheeler, 1964;Schafer et al, 1975Schafer et al, , 1977Schafer et al, , 1978Andreoli et al, 1978;Bishop et al, 1979;Hill, 1980;Berry, 1983;Spring, 1983). In some tissues (e.g., Necturu.s gallbladder), a great deal is known about the routes, mechanisms, and properties of salt transport systems (Baerentsen et al, 1983;Reuss, 1983Reuss, , 1984Reuss, , 1989Reuss and Costantin, 1984;Weinman and Reuss, 1984;Reuss and Stoddard, 1987); however, there is less information about the water transport pathway(s).…”

Section: Introductionmentioning

confidence: 99%

Osmotic water permeability of Necturus gallbladder epithelium.

Cotton

Weinstein

Reuss

1989

The Journal of General Physiology

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An electrophysiological technique that is sensitive to small changes in cell water content and has good temporal resolution was used to determine the hydraulic permeability (Lp) of Necturus gallbladder epithelium. The epithelial cells were loaded with the impermeant cation tetramethylammonium (TMA+) by transient exposure to the pore-forming ionophore nystatin in the presence of bathing solution TMA+. Upon removal of the nystatin a small amount of TMA+ is trapped within the cell. Changes in cell water content result in changes in intracellular TMA+ activity which are measured with intracellular ion-sensitive microelectrodes. We describe a method that allows us to determine the time course for the increase or decrease in the concentration of osmotic solute at the membrane surface, which allows for continuous monitoring of the difference in osmolality across the apical membrane. We also describe a new method for the determination of transepithelial hydraulic permeability (Ltp). Apical and basolateral membrane Lp's were assessed from the initial rates of change in cell water volume in response to anisosmotic mucosal or serosal bathing solutions, respectively. The corresponding values for apical and basolateral membrane Lp's were 0.66 x 10(-3) and 0.38 x 10(-3) cm/s.osmol/kg, respectively. This method underestimates the true Lp values because the nominal osmotic differences (delta II) cannot be imposed instantaneously, and because it is not possible to measure the true initial rate of volume change. A model was developed that allows for the simultaneous determination of both apical and basal membrane Lp's from a unilateral exposure to an anisosmotic bathing solution (mucosal). The estimates of apical and basal Lp with this method were 1.16 x 10(-3) and 0.84 x 10(-3) cm/s.osmol/kg, respectively. The values of Lp for the apical and basal cell membranes are sufficiently large that only a small (less than 3 mosmol/kg) transepithelial difference in osmolality is required to drive the observed rate of spontaneous fluid absorption by the gallbladder. Furthermore, comparison of membrane and transepithelial Lp's suggests that a large fraction of the transepithelial water flow is across the cells rather than across the tight junctions.

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“…This is a very surprising result because for a leaky epithelium there should be tracer fluxes in both directions and this has been observed in other studies. For instance the tracer fluxes have been shown to be several fold larger than the net fluxes for proximal tubules of the kidney [488–491] and the choroid plexuses of bullfrogs [492, 493]. Smith and Rapoport [261] and Murphy and Johanson [265] reported tracer Na + flux towards CSF in the rat of 2.3% min −1 (relative to Na + content of the CSF) but did not report net CSF secretion rates.…”

mentioning

confidence: 99%

Fluid and ion transfer across the blood–brain and blood–cerebrospinal fluid barriers; a comparative account of mechanisms and roles

Hladky

Barrand

2016

Fluids Barriers CNS

230

253

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The two major interfaces separating brain and blood have different primary roles. The choroid plexuses secrete cerebrospinal fluid into the ventricles, accounting for most net fluid entry to the brain. Aquaporin, AQP1, allows water transfer across the apical surface of the choroid epithelium; another protein, perhaps GLUT1, is important on the basolateral surface. Fluid secretion is driven by apical Na+-pumps. K+ secretion occurs via net paracellular influx through relatively leaky tight junctions partially offset by transcellular efflux. The blood–brain barrier lining brain microvasculature, allows passage of O2, CO2, and glucose as required for brain cell metabolism. Because of high resistance tight junctions between microvascular endothelial cells transport of most polar solutes is greatly restricted. Because solute permeability is low, hydrostatic pressure differences cannot account for net fluid movement; however, water permeability is sufficient for fluid secretion with water following net solute transport. The endothelial cells have ion transporters that, if appropriately arranged, could support fluid secretion. Evidence favours a rate smaller than, but not much smaller than, that of the choroid plexuses. At the blood–brain barrier Na+ tracer influx into the brain substantially exceeds any possible net flux. The tracer flux may occur primarily by a paracellular route. The blood–brain barrier is the most important interface for maintaining interstitial fluid (ISF) K+ concentration within tight limits. This is most likely because Na+-pumps vary the rate at which K+ is transported out of ISF in response to small changes in K+ concentration. There is also evidence for functional regulation of K+ transporters with chronic changes in plasma concentration. The blood–brain barrier is also important in regulating HCO3 − and pH in ISF: the principles of this regulation are reviewed. Whether the rate of blood–brain barrier HCO3 − transport is slow or fast is discussed critically: a slow transport rate comparable to those of other ions is favoured. In metabolic acidosis and alkalosis variations in HCO3 − concentration and pH are much smaller in ISF than in plasma whereas in respiratory acidosis variations in pHISF and pHplasma are similar. The key similarities and differences of the two interfaces are summarized.

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Fluid absorption and active and passive ion flows in the rabbit superficial pars recta

Cited by 21 publications

References 0 publications

Renal water reabsorption: A physiologic retrospective in a molecular era

Renal water reabsorption: A physiologic retrospective in a molecular era

Osmotic water permeability of Necturus gallbladder epithelium.

Fluid and ion transfer across the blood–brain and blood–cerebrospinal fluid barriers; a comparative account of mechanisms and roles

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