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PubMed2004

Aquaporin 6 is permeable to glycerol and urea.

The passive water permeability ( L(p)) of AQP6 is activated by Hg(2+). Our aim was to test if L(p) was associated with a permeability to small hydrophilic molecules such as glycerol and urea. AQP6 was expressed in Xenopus laevis oocytes and activated by 0.3 mM of HgCl(2) in the bathing solution. HgCl(2) caused the oocytes to swell at a rate of about 0.3% min(-1). The L(p) of AQP6 was determined from brief additions or removals of mannitol from the bathing solution, and compared to the L(p) obtained from adding glycerol or urea. In paired experiments, L(p (mannitol)) was 2.4+/-0.1, L(p (glycerol)) 1.5+/-0.2, and L(p (urea)) 0.7+/-0.1 (units: 10(-5) cm s(-1) osmol(-1); 14 oocytes); the latter was not different from L(p)s obtained for native oocytes. The L(p)s were independent of the Hg(2+)-induced swelling and of the magnitude of the osmotic challenge (-75 to +100 mosmol). Hg(2+) stimulated the uptake of [(14)C]glycerol fivefold and [(14)C]urea twofold in AQP6-expressing oocytes. There were no significant uptakes in native oocytes nor in AQP1-expressing oocytes whether these were treated with HgCl(2) or not. We conclude that water, glycerol and urea share an aqueous pathway in AQP6.

Algorithms↗

PubMed1978

Circulatory effects on osmotic water exchange in Rana pipiens.

Tritiated water (3H2O) exchange was shown to be more sensitive to circulatory changes than to arginine vasopressin (ADH)-induced permeability changes. Reducing the circulation (sciatic artery ligation) and increasing the circulation (severing the sciatic nerve) caused the 3H2O exchange in frog legs to decrease from 6.0 +/- 1.3 (5) to 3.5 +/- 0.5 and increase from 6.0 +/- 0.7 (10) to 8.6 +/- 0.6 ml.h-1, respectively. In contrast injection of ADH caused a negligible increase in 3H2O exchange from whole frogs, while at the same time causing a significant increase in osmotic water exchange from 0.22 +/- 0.08 (6) to 0.63 +/- 0.13 (6) g.100 cm-2.h-1.200 mosM-1. Circulatory changes in whole frogs were produced by inducing a diving bradycardia that was less pronounced in a bath aerated with oxygen than with air. The bradycardia caused a reduction in skin circulation, as measured by 3H2O exchange, from 0.210 +/- 0.007 (16) to 0.17 +/- 0.006 (16) ml.h-1.cm-2 in air mixed media and from 0.149 +/- 0.009 (16) to 0.135 +/- 0.011 (16) in oxygen mixed media. Diving bradycardia was also found to affect osmotic water uptake which decreased from 0.61 +/- 0.05 (16) to 0.39 +/- 0.03 (16) g.100 cm-2.h-1.200 mosM-1 in air mixed media and from 0.61 +/- 0.05 (16) to 0.51 +/- 0.04 (16) in oxygen mixed media. The results indicate that circulation affects osmotic water exchange.

Animals↗

PubMed1992

Water handling in the rat jejunum: effects of acidification of the medium.

The minute-by-minute net water movement (Jw) in the rat jejunum was studied in relation to the diffusive water (Pw) and mannitol (Ps) permeabilities with the following results. (a) Jw was a linear function of the applied hydrostatic and osmotic transepithelial gradients (hydrostatic permeability coefficient, Phydr = 0.052 +/- 0.011 cm s-1; osmotic permeability coefficient, Posm = 0.0069 +/- 0.0014 cm s-1. (b) A fraction of this absorptive Jw (transport-associated Jw, Jwt = 0.086 +/- 0.024 microliter min-1 cm-2) was independent of the presence of any osmotic, hydrostatic or chemical gradient. (c) In the absence of Na+, Jwt was not significantly different from zero and there was an increase in Phydr but no change in Posm. (d) In the presence of a hydrostatic gradient (10 cm H2O, mucosal side), acidification of the medium (95% CO2 bubbling, pH 6.2) simultaneously and reversibly increased Jw and decreased Pw. (e) When an osmotic gradient was present (40 mM polyethyleneglycol on the serosal side) a net increase in Jw was observed. CO2 bubbling in these conditions reversibly reduced Jw while increasing Ps. (f) These effects were not observed when the serosal or mucosal pH was reduced in the presence of a nonpermeant buffer (HEPES/TRIS; MES/TRIS). If we accept that Ps is a good marker of paracellular movements and that Pw mainly reflects transcellular water movements, we may conclude that acidification of the medium, in the presence of bicarbonate, modifies both paracellular and transcellular routes. The experimental evidence indicates that an increase in proton concentration opens the paracellular pathway and probably has a blocking effect on a transcellular route.

Animals↗

PubMed1979

Osmotic water flow in leaky epithelia.

I review three currently unsolved and controversial problems in understanding solute-linked water transport in epithelia. 1. Values of osmotic water permeability (Posm) calculated from steady-state osmotic flow in response to a gradient of a probe molecule tend to be underestimates, because of three unstirred-layer (USL) effects. These are: dissipation of the probe's gradient by diffusion in USL's; reduction of the probe's gradient, due to the sweeping-away effect of water flow generated by the probe itself; and solute polarization (creation of an opposing gradient of an initially symmetrically distributed solute by the sweeping-away effect). These errors increase with probe permeability, USL thickness, Posm, and concentration ratio of symmetrically distributed solute to probe, and vary inversely as the fractional area available for water flow (e.g., lateral intercellular space width). The form of an osmotic transient, and the possibility of extracting a true Posm value from the transient, depend on the relative values of three time constants: those for solute diffusion in USL's, for solute polarization by water flow in USL's and for measuring water flow. Sweeping-away effects cause major underestimates (by one or more orders of magnitude) in epithelial Posm determinations, as shown by apparent streaming potentials during osmotic flow and by transiently reversed flows after removal of the proble. True Posm values for leaky epithelia probably exceed 10(-3) or 10(-2) cm/sec.osm. The necessary conditions for resolving osmotic transients are set out. 2. I illustrate the difficulties in deciding what fraction of transepithelial water flow is via the cells, and what fraction via the junctions. There is no existing method for answering this question. 3. Controversies about the validity, or need for modification, of the standing-gradient theory are discussed. Progress in this field requires new methods: to resolve osmotic transients; to separate transcellular and transjunctional water flows; and to measure solute concentrations in lateral intercellular spaces directly.

Animals↗

PubMed1969

The effect of amphotericin B on the water and nonelectrolyte permeability of thin lipid membranes.

This paper reports the effects of amphotericin B, a polyene antibiotic, on the water and nonelectrolyte permeability of optically black, thin lipid membranes formed from sheep red blood cell lipids dissolved in decane. The permeability coefficients for the diffusion of water and nonelectrolytes (P(DDi)) were estimated from unidirectional tracer fluxes when net water flow (J(w)) was zero. Alternatively, an osmotic water permeability coefficient (P(f)) was computed from J(w) when the two aqueous phases contained unequal solute concentrations. In the absence of amphotericin B, when the membrane solutions contained equimolar amounts of cholesterol and phospholipid, P(f) was 22.9 +/- 4.6 microsec(-1) and P(DDHDH2O) was 10.8 +/- 2.4 microsec(-1). Furthermore, P(DDi) was < 0.05 microsec(-1) for urea, glycerol, ribose, arabinose, glucose, and sucrose, and sigma(i), the reflection coefficient of each of these solutes was one. When amphotericin B (10(-6)M) was present in the aqueous phases and the membrane solutions contained equimolar amounts of cholesterol and phospholipid, P(DDHDH2O) was 18.1 +/- 2.4 microsec(-1); P(f) was 549 +/- 143 microsec(-1) when glucose, sucrose, and raffinose were the aqueous solutes. Concomitantly, P(DDi) varied inversely, and sigma(i) directly, with the effective hydrodynamic radii of the solutes tested. These polyene-dependent phenomena required the presence of cholesterol in the membrane solutions. These data were analyzed in terms of restricted diffusion and filtration through uniform right circular cylinders, and were compatible with the hypothesis that the interactions of amphotericin B with membrane-bound cholesterol result in the formation of pores whose equivalent radii are in the range 7 to 10.5 A.

Amides↗

PubMed1997

Aquaporin-2 transfection of Madin-Darby canine kidney cells reconstitutes vasopressin-regulated transcellular osmotic water transport.

Water transport across the mammalian collecting tubule is regulated by vasopressin-dependent aquaporin-2 insertion into and retrieval from the apical cell membrane. To establish a cell line that properly expresses aquaporin-2 and its hormone-dependent shuttling, Madin-Darby canine kidney cells were stably transfected with an aquaporin-2 expression construct. Cells of a representative clone (wild-type 10 [WT-10]) were grown on semipermeable supports, and transcellular osmotic water permeability (Pf; in microm/s +/- SEM) was measured. The basal Pf of WT-10 cells, which was lowered with indomethacin, increased from 10.6 +/- 0.8 to 35.7 +/- 1.2 upon incubation with 1-desamino-8-D-arginine vasopressin (dDAVP). This increase coincided with the translocation of aquaporin-2 from an intracellular compartment to the apical membrane. The Pf of untransfected cells (6.5 +/- 0.8) was unchanged by dDAVP. Kinetic studies with WT-10 cells revealed that maximal Pf was obtained within 30 min after dDAVP addition, which remained elevated for at least 90 min. Intracellular cAMP levels peaked within 5 min after dDAVP admission and decreased to basal levels within 45 min. After preincubation with dDAVP, the Pf decreased within 15 min after dDAVP washout and returned to basal levels within 75 min. In conclusion, the WT-10 cells mimic the vasopressin-regulated transcellular water transport and aquaporin-2 translocation as found in collecting duct cells to a great extent, and therefore constitute an in vitro cell model that can be used to study the regulation of transcellular water transport in detail and provide a simplified test system for screening putative aquaporin-2 blockers.

Animals↗

PubMed1989

Functional colocalization of water channels and proton pumps in endosomes from kidney proximal tubule.

The apical membrane of mammalian proximal tubule undergoes rapid membrane cycling by exocytosis and endocytosis. Osmotic water and ATP-driven proton transport were measured in endocytic vesicles from rabbit and rat proximal tubule apical membrane labeled in vivo with the fluid phase marker fluorescein-dextran. Osmotic water permeability (Pf) was determined from the time course of fluorescein-dextran fluorescence after exposure of endosomes to an inward osmotic gradient in a stopped-flow apparatus. Pf was 0.009 (rabbit) and 0.029 cm/s (rat) (23 degrees C) and independent of osmotic gradient size. Pf in rabbit endosomes was inhibited reversibly by HgCl2 (KI = 0.2 mM) and had an activation energy of 6.4 +/- 0.5 kcal/mol (15-35 degrees C). Endosomal proton ATPase activity was measured from the time course of internal pH, measured by fluorescein-dextran fluorescence, after the addition of external ATP. Endosomes contained an ATP-driven proton pump that was sensitive to N-ethylmaleimide and insensitive to vanadate and oligomycin. In response to saturating [ATP] the pump acidified the endosomal compartment at a rate of 0.17 (rat) and 0.029 pH unit/s (rabbit); at an external pH of 7.4, the steady-state pH was 6.4 (rat) and 6.5 (rabbit). To examine whether water channels and the proton ATPase were present in the same endosome, the time course of fluorescein-dextran fluorescence was measured in response to an osmotic gradient in the presence and absence of ATP. ATP did not alter endosome Pf, but decreased the amplitude of the fluorescence signal by 43 +/- 3% (rabbit) and 47 +/- 4% (rat).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Glucose transporters do not serve as water channels in renal and intestinal epithelia.

Glucose carriers have been shown to serve as water channels in macrophages and in oocytes injected with messenger ribonucleic acid (mRNA) encoding the glucose carrier protein (Fischbarg et al. The contribution, therefore, of glucose carriers to osmotic water permeability (Pf) in renal and intestinal epithelial cells was investigated. Pf of brush border membrane vesicles (BBMVs) and of basolateral membrane vesicles (BLMVs) was studied using stopped-flow spectrophotometry. Osmotic shrinkage of renal vesicles exhibited fast and slow components at 4 degrees C and 37 degrees C. The fast component could be inhibited by HgCl2 or dimethylsulphoxide (DMSO) at these temperatures, whereas the slow component was inhibited only at 4 degrees C. Osmotic shrinkage of intestinal BBMVs and BLMVs was homogeneous at 4 degrees C and 37 degrees C and was slightly inhibitable by HgCl2 or DMSO at 4 degrees C but not 37 degrees C. In both tissues, vesicle uptake of glucose was sensitive to HgCl2, but not to DMSO. Phlorizin and phloretin inhibited D-glucose uptake in BBMVs and BLMVs respectively, but had no significant effect on Pf. In membrane vesicles of kidney origin, Pf was tenfold higher than in membranes from intestine. This difference was not reflected by the phlorizin- and phloretin-sensitive D-glucose uptakes. Our study concludes that glucose transporters do not serve as water channels in kidney or intestine. Although membrane proteins contribute slightly to Pf at 4 degrees C, this contribution is insignificant at 37 degrees C. A membrane protein serving specifically as a water channel could only be demonstrated in renal cortical membranes.

Alanine↗

PubMed2006

Hepatocyte growth factor attenuates cerebral ischemia-induced increase in permeability of the blood-brain barrier and decreases in expression of tight junctional proteins in cerebral vessels.

Hepatocyte growth factor (HGF) exerts its physiological activities as that of an organotropic factor for regeneration and can prevent ischemia-induced injuries; however, its effect and mechanism of action under in vivo pathophysiological conditions remains to be determined. Recently, we demonstrated that treatment with human recombinant HGF (hrHGF) attenuated the disruption of the blood-brain barrier (BBB) observed after microsphere embolism-induced sustained cerebral ischemia. To see if tight junctional proteins were involved in this attenuation, in the present study, we investigated the effects of HGF on the levels of occludin and zonula occludens (ZO)-1 in cerebrovascular endothelial cells after microsphere embolism. Sustained cerebral ischemia was induced by the injection of 700 microspheres (48 microm diameter) into the right internal carotid artery of rats. hrHGF was injected into the right ventricle of the brain by using an osmotic pump at a dose of 30 microg/7 days per animal. The levels of tight junctional proteins in the endothelial cells were examined by immunohistochemical analysis. Treatment with hrHGF attenuated the decrease in the expression of occludin and ZO-1 proteins in the endothelial cells that occurred after sustained cerebral ischemia. Furthermore, treatment with hrHGF resulted in retention of these tight junctional proteins in fluorescein isothiocyanate (FITC)-albumin-perfused cerebral vessels, which did not leak FITC-albumin in the ipsilateral cortex. These results suggest that HGF-mediated maintenance of the tight junctional proteins in the endothelial cells may be a possible mechanism for the protective effect of HGF against the disruption of the BBB after cerebral ischemia.

Animals↗

PubMed1992

Cytoplasmic dilution induces antidiuretic hormone water channel retrieval in toad urinary bladder.

Antidiuretic hormone (ADH) increases the osmotic water permeability (Pf) of the toad urinary bladder by insertion of water channels into the apical cell membrane. Transepithelial water flow (Jv) reduces Pf by inducing endocytosis of apical water channels despite continuous ADH stimulation. This phenomenon is termed flux inhibition. We wished to determine whether cytoplasmic dilution or transcellular Jv causes flux inhibition because both have been proposed previously as a primary regulatory mechanism for this process. Apical membrane endocytosis was quantified by monitoring the uptake of the fluid phase marker fluorescein isothiocyanate dextran (FITC-dextran). FITC-dextran fluorescence was monitored in Triton X-100 extracts of epithelial cells as the ratio of total tissue fluorescence compared with background fluorescence. The background was defined as cellular autofluorescence and nonspecific tissue staining due to the presence of small amounts of free fluorescein contaminating the FITC-dextran. FITC-dextran uptake measured under symmetric isotonic (220 mosmol/kgH2O) conditions in either the absence (1.0 +/- 0.4 SD; n = 14) or presence (1.3 +/- 0.3; n = 4) of ADH was not statistically different from that of background. In contrast, flux inhibition induced by a 180 mosmol/kgH2O apical-to-basolateral osmotic gradient increased FITC-dextran uptake to 3.4 +/- 1.3 (n = 7). FITC-dextran uptake was identical in bladders exposed to symmetric hypotonic (150 mosmol/kgH2O) solutions during ADH (3.6 +/- 0.9; n = 6) or adenosine 3',5'-cyclic monophosphate (3.1 +/- 0.4 fold; n = 3) stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2005

Electrical parameters and water permeability properties of monolayers formed by T84 cells cultured on permeable supports.

T84 is an established cell line expressing an enterocyte phenotype whose permeability properties have been widely explored. Osmotic permeability (POSM), hydraulic permeability (PHYDR) and transport-associated net water fluxes (JW-transp), as well as short-circuit current (ISC), transepithelial resistance (RT), and potential difference (deltaVT) were measured in T84 monolayers with the following results: POSM 1.3 +/- 0.1 cm.s-1 x 10-3; PHYDR 0.27 +/- 0.02 cm.s-1; RT 2426 +/- 109 omega.cm2, and deltaVT 1.31 +/- 0.38 mV. The effect of 50 microM 5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazol-2-one (DCEBIO), a "net Cl- secretory agent", on T84 cells was also studied. We confirm the reported important increase in ISC induced by DCEBIO which was associated here with a modest secretory deltaJW-transp. The present results were compared with those reported using the same experimental approach applied to established cell lines originating from intestinal and renal epithelial cells (Caco-2, LLC-PK1 and RCCD-1). No clear association between PHYDR and RT could be demonstrated and high PHYDR values were observed in an electrically tight epithelium, supporting the view that a "water leaky" barrier is not necessarily an "electrically leaky" one. Furthermore, the modest secretory deltaJW-transp was not consistent with previous results obtained with RCCD-1 cells stimulated with vasopressin (absorptive fluxes) or with T84 cells secreting water under the action of Escherichia coli heat stable enterotoxin. We conclude that, while the presence of aquaporins is necessary to dissipate an external osmotic gradient, coupling between water and ion transport cannot be explained by a simple and common underlying mechanism.

Cell Line↗

PubMed1976

Physiology of salivary secretion.

The aim of the present work was to explain the mechanism of the acinar secretion of the salivary gland during stimulation. The following items were discussed and concluded. (1) The acinus is the majority of cells being the powerful transport system of the fluid from interstitial side to lumen. (2) Osmotic flow was clarified being a cause of water transport, in which the osmolality gradient across the acinus epithelium was initiated by a preceded salt transport. (3) The grades of osmotic gradient, of hydraulic conductivity, and of semipermeable property of gland epithelia were described. (4) On salt transport during stimulation, Na+ inflow across the basal plasma membrane and Na+ extrusion across the luminal membrane of the acinus cell were discussed with respect to the electrochemical gradient and ionic flow. From the electrophysiological work and the ionic distribution of the salivary gland, it is concluded that massive Na+ inflow and K+ outflow across the basal plasma membrane was a passive process due to an increase of permeability to those ion during stimulation, but the process of Na+ extrusion across the plasma membranes of the luminal side of the cell as well as of the secretory granules was active. (5) The electrochemical gradient for Na+ and K+ at the basal plasma membrane which had an important role for passive Na+ and K+ transport may be maintained by ouabain-sensitive Na+-K+ pump as most other cells. (6) A model for salt transport across the acinar cell was proposed. Intracellular Na+ due to passive Na+ inflow may activate cooperatively the Na(Cl) transport system at luminal plasma membrane and membrane of secretory granules in high levels of (Na+)in. Though it also activated the Na+ -K+ transport at the basal plasma membrane in any level of (Na+)in. (7) Energetics for the ion transport of gland was discussed with a transport-work rate equation as well as oxygen consumption in secretory state. It is assumed that the energy in active transport at the luminal plasma membrane requires more than the dissipated energy in passive process at the basal plasma membrane. The energy for active transport across the luminal plasma membrane may be corresponded to a main part of oxygen consumption for ion transport across the overall epithelium. (8) The phenomena of osmotic flow coupling with salt flow and of passive ionic flow coupling with electrochemical gradient which is maintained by Na+ -K+ pump may be an expression of production and utilization of negative entropy which is a characteristic of biological membrane.

Animals↗

PubMed2003

Hypothyroidism increases osmotic water permeability (Pf) in the developing renal brush border membrane.

The osmotic water permeability (Pf) of the rabbit proximal tubule brush border membrane vesicles (BBMV) increases during maturation and is mediated by an increase in aquaporin-1 (AQP1) protein expression. Serum thyroid hormone levels increase after birth and have been shown to play a role in the maturation of other renal transport functions. We examined the hypothesis that thyroid hormone plays a role in the maturational increase in osmotic water permeability. Hypothyroidism was induced by addition of 0.1% propylthiouracil (PTU) to the drinking water of pregnant rabbits (starting 9 d before delivery) and was continued until the rabbits were studied as adults (9-11 wk). Some animals received thyroid hormone replacement by daily injection with triiodothyronine (T3; 10 microg/100 g body weight) for three days before study. Pf was found to be higher in BBMV from hypothyroid (82.7 +/- 5.5 microm/s) than from euthyroid (60.6 +/- 4.0 microm/s) and T3-replacement rabbits (69.0 +/- 5.0 microm/s) (p < 0.05). The activation energy (Ea; in kcal/deg.mol) of Pf was not different among the three experimental groups (euthyroid 5.6 +/- 0.9, hypothyroid 4.9 +/- 0.8, T3-replacement 5.0 +/- 1.0; p = NS), nor was the percentage mercury inhibition of Pf (euthyroid 66.5 +/- 5.3, hypothyroid 74.2 +/- 3.2 and T3-replacement 73.1 +/- 4.3; p = NS). AQP1 expression, measured by immunoblotting, was highest in BBMV from hypothyroid rabbits (p < 0.05). Membrane fluidity, measured as steady-state generalized polarization (GP) of Laurdan, which is inversely related to membrane fluidity, was significantly different between the three groups (GP: euthyroid 0.307 +/- 0.004, hypothyroid 0.271 +/- 0.004 and T3-replacement 0.287 +/- 0.003; for all p < 0.05). These data demonstrate that the maturational increase in thyroid hormone levels is not responsible for the maturational increase in water transport. Surprisingly, congenital hypothyroidism in rabbits is associated with an increased Pf when rabbits are studied as adults. The higher Pf in hypothyroid adult rabbits is due to a higher expression of AQP1 protein as well as a greater membrane fluidity than in euthyroid rabbits.

Animals↗

PubMed2002

Aquaporin deletion in mice reduces corneal water permeability and delays restoration of transparency after swelling.

Two aquaporin (AQP)-type water channels are expressed in mammalian cornea, AQP1 in endothelial cells and AQP5 in epithelial cells. To test whether these aquaporins are involved in corneal fluid transport and transparency, we compared corneal thickness, water permeability, and response to experimental swelling in wild type mice and transgenic null mice lacking AQP1 and AQP5. Corneal thickness in fixed sections was remarkably reduced in AQP1 null mice and increased in AQP5 null mice. By z-scanning confocal microscopy, corneal thickness in vivo was (in microm, mean +/- S.E., n = 5 mice) 123 +/- 1 (wild type), 101 +/- 2 (AQP1 null), and 144 +/- 2 (AQP5 null). After exposure of the external corneal surface to hypotonic saline (100 mosm), the rate of corneal swelling (5.0 +/- 0.3 microm/min, wild type) was reduced by AQP5 deletion (2.7 +/- 0.1 microm/min). After exposure of the endothelial surface to hypotonic saline by anterior chamber perfusion, the rate of corneal swelling (7.1 +/- 1.0 microm/min, wild type) was reduced by AQP1 deletion (1.6 +/- 0.4 microm/min). Base-line corneal transparency was not impaired by AQP1 or AQP5 deletion. However, the recovery of corneal transparency and thickness after hypotonic swelling (10-min exposure of corneal surface to hypotonic saline) was remarkably delayed in AQP1 null mice with approximately 75% recovery at 7 min in wild type mice compared with 5% recovery in AQP1 null mice. Our data indicate that AQP1 and AQP5 provide the principal routes for corneal water transport across the endothelial and epithelial barriers, respectively. The impaired recovery of corneal transparency in AQP1 null mice provides evidence for the involvement of AQP1 in active extrusion of fluid from the corneal stroma across the corneal endothelium. The up-regulation of AQP1 expression and/or function in corneal endothelium may reduce corneal swelling and opacification following injury.

Animals↗

PubMed1996

Nitric oxide inhibits ADH-stimulated osmotic water permeability in cortical collecting ducts.

Nitric oxide (NO) reduces blood pressure in vivo by two mechanisms, vasodilation and increasing urinary volume: however, the exact mechanism by which it increases urinary volume is not clear. We hypothesized that NO inhibits antidiuretic hormone (ADH)-stimulated fluid reabsorption (J(r)) by the isolated rat cortical collecting duct (CCD) by decreasing water permeability (Pf) and sodium reabsorption (Jna). In the presence of 10(-11) MADH, Jv was 0.15 +/- 0.04 nl.min-1.mm-1; after 10(-6) M spermine nonoate (SPM) was added to the bath. Jv decreased to 0.06 +/- 0.03 nl.min-1.mm-1 (P < 0.03). To investigate whether the inhibition of Jv was the result of decreased Pf and/or Jna, we first tested the effect of SPM on ADH-stimulated Pf. Basal Pf was stimulated to 289.2 +/- 77.3 microns/s after 10(-11) M ADH was added to the bath (P < 0.01). SPM decreased Pf to 159.8 +/- 45.0 microns/s (P < 0.05). To ensure that this effect on Pf was due to NO release, we used another NO donor, nitroglycerin (NTG). Pf was initially -25.8 +/- 18.3 microns/s and increased to 133.9 +/- 30.5 microns/s after addition of 10(-11) M ADH (P < 0.002). NTG, 20 microM, lowered Pf to 92.4 +/- 18.4 microns/s (P < 0.02). In the presence of 10(-9) M ADH, NTG also decreased Pf(P < 0.04). Next we investigated the effect of SPM on ADH-stimulated JNa. In the presence of ADH, JNa was 37.8 +/- 7.3 pmol.min-1.mm-1. After SPM was added, it dropped to 24.3 +/- 5.1 pmol.min-1.mm-1 (P < 0.05). Time controls exhibited no change in ADH-stimulated Jv, Pf, or Jna. We concluded that 1) NO decreases ADH-stimulated water and sodium transport in the isolate CCD, and 2) water reabsorption is inhibited by a primary effect on Pf. A direct effect of NO on the CCD may explain its natriuretic and diuretic effects observed in vivo.

Animals↗

PubMedDate not supplied

Effects of frog-skin angiotensin II in amphibians.

The role of frog-skin angiotensin II (AII) in amphibia was studied by comparing the sodium and water permeability effects of three angiotensins (AII): frog skin (Ala-Pro-Gly-[Ile3, Val5]-Ang II), human [( Asp1, Ile5]-AII), and Japanese goosefish [( Asn1-Val5]-AII). Frog-skin AII increased the short-circuit current (SCC) significantly after it was added to the dermal side of the isolated skin of the South American frogs, Leptodactylus chaquensis and ocellatus, and the toad, Bufo arenarum, in concentrations of 10(-6) M. In frogs, the effect was significant at 15 minutes and reached 45% over control after 2 1/2 hours. The effect cannot be achieved with concentrations lower than 10(-7) M. Since amiloride (10(-4) M) blocked the SCC response, and absence of chloride in the bathing fluid did not, the effect is probably dependent on sodium transport. Human AII (10(-6) M) produced a similar response in summer frogs that had been treated with 0.1% NaCl for 14 days. Goosefish AII was ineffective at similar concentrations, and none of the angiotensins modified SCC in the toad bladder. Hydrosmotic effects could be achieved with the three angiotensins, the response being dependent on seasonal and species factors but always considerably lower than that of the neurohypophyseal peptides. Vascular reactivity of the isolated frog hindlimbs was compared by dose-response curves. Potency ratios on a molar basis against frog-skin AII was 1.136 for human AII and 1.193 for goosefish AII. The results show that the effects of the angiotensins differ in both the response of SCC to frog-skin angiotensin and its higher vascular effects.

Amphibians↗

PubMed2005

Cutaneous metabolism of a dipeptide influences the iontophoretic flux of a concomitant uncharged permeant.

Passive and iontophoretic transport of the model dipeptide tyrosine-phenylalanine (TyrPhe) that is subject to cutaneous metabolism and the uncharged glucose derivative benzyl-2-acetamido-2-deoxy-alpha-d-glucopyranoside (BAd-alpha-Glc) used as electroosmosis marker through heat-separated human epidermis was investigated in vitro. TyrPhe and BAd-alpha-Glc were used separately and in combination in order to determine their interaction in terms of permeability and the influence of skin metabolism of TyrPhe on permeation rate and tissue retention of itself and of BAd-alpha-Glc. TyrPhe was chemically and electrochemically stable but underwent considerable degradation in the epidermis under reflection boundary conditions with generation of degradation products tyrosine (Tyr) and phenylalanine (Phe) confirming cutaneous metabolism of TyrPhe in heat-separated human epidermis, which was more pronounced at pH 4.5 than at pH 3.0. As a result, no reproducible epidermis permeation of TyrPhe at pH 3 and no permeation at all at pH 4.5 was measured regardless of the presence of BAd-alpha-Glc, accompanied by increased levels of Tyr and Phe compared to blank runs. Low temperature (4 degrees C) at both pH values and addition of o-phenanthroline at pH 3 but not at pH 4.5 yielded reproducible TyrPhe permeation and blank, i.e., endogenous levels of Tyr and Phe evidencing inhibition of degradation. Constant voltage anodal iontophoresis marginally reduced BAd-alpha-Glc flux at pH 3 and 4.5 compared to the passive flux. In combination with TyrPhe, iontophoretic flux of BAd-alpha-Glc was increased markedly compared to the passive one when TyrPhe was metabolized in the tissue, while no such increase was observed when TyrPhe metabolism was inhibited. The increase of BAd-alpha-Glc iontophoretic flux was accompanied by a considerable decrease of the BAd-alpha-Glc amount retained in the epidermis. The presence of the generated Tyr and Phe, therefore, appears to be related to a decrease of the BAd-alpha-Glc amount retained in the epidermis upon application of an electrical voltage and an enhancement of its iontophoretic flux. Thus, an interaction between the concurrent permeants at the level of tissue retention induced by metabolism can influence the apparent iontophoretic permeation.

Dipeptides↗

PubMed2004

Single-step, self-etch adhesives behave as permeable membranes after polymerization. Part III. Evidence from fluid conductance and artificial caries inhibition.

PURPOSE: To test the hypothesis that formation of inhibition zones by bonded restorations in artificially-induced carious dentin lesions is related to the permeability of the self-etch adhesives. METHODS: Fluid conductance of four single-step self-etch adhesives (Prompt L-Pop, Etch&Prime 3.0, One-Up Bond F and Reactmer Bond), and a control two-step self-etch adhesive (UniFil Bond) were measured after sound dentin surfaces were:(1) acid-etched; (2) polished to produce smear layers; (3) bonded with the adhesive; each at 20 cm hydrostatic pressure (hp). Osmotic fluid conductance was also determined for the bonded dentin after immersion in 4.8 M CaCl2 at 0 cm hp. For artificial caries inhibition, a non-fluoride releasing (NFR) two-step self-etch adhesive (UniFil Bond) and a fluoride-releasing (FR) single-step adhesive (Reactmer Bond) were used in combination with a NFR composite (Metafil CX) or a FR restorative material (Reactmer Paste). Artificial caries were induced in these restorations, from which 120 +/- 10 microm thick sections and the effect of caries inhibition were quantitatively assessed with polarizing light microscopy and image analysis. RESULTS: Fluid conductance after bonding with the single-step adhesives Prompt L-Pop and Etch&Prime 3.0 were not significantly different from those recorded from smear layer-covered dentin. Although better seals were achieved with One-Up Bond F and Reactmer Bond, fluid conductance at 20 cm hp was significantly higher than the two-step self-etch adhesive UniFil Bond. Osmotic conductance at 0 cm hp were not significantly different from normal fluid conductance at 20 cm hp. The sizes of artificial carious lesions in UniFil Bond were significantly higher irrespective of whether a FR or NFR composite was used. Significant reduction in lesion size occurred in Reactmer Bond with the use of a NFR composite, and even more so with the use of a FR composite.

Acid Etching, Dental↗