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PubMed1978

Effect of hyperosmolar stimuli and coeliac disease on the permeability of the human gastrointestinal tract.

1. Oral loads have been used to assess the permeability of the human gastrointestinal tract, with lactulose (mol. wt. 342), raffinose (mol. wt. 504), stachyose (mol. wt. 666) and a fluoresceinlabelled dextran (mol. wt. 3000) as marker substances. Timed urinary recovery of these substances, which are not metabolized, was measured by quantitative paper chromatography and direct fluorimetry, and the results were used as an indication of passive intestinal permeability. 2. Results in healthy adults showed that permeability to these markers was dependent on molecular size, even after correction for aqueous diffusion differences, such that a profile of restricted permeability could be described for this range of markers. Interpretation in terms of conventional pore theory suggested the presence of more than one population of pores. 3. Ingestion of solutions made hyperosmotic by inclusion of glycerol resulted in a large increase in permeability, in a pattern that suggested an increase in either the size or frequency of a range of smaller pores. 4. A similar increase in permeability and alteration in the profile of restriction was found in patients with coeliac disease. 5. The possible location of such pores in the gastrointestinal mucosa is discussed in relation to the cell membrane, the intercellular junction, and the sites of cell exfoliation.

Celiac Disease↗
PubMed1992

Effects of spermine on water absorption, polyethylene glycol 4000 permeability and collagenase activity in rat descending colon in vivo.

1. The effects of spermine in the concentration range 0-10 mmol/l on (a) the fluid absorption, (b) the polyethylene glycol permeability, (c) the release of collagenase activity activity into the lumen and (d) the histological appearance of rat descending colon were examined. 2. Spermine (5 mmol/l) decreased fluid absorption from 48.83 +/- 2.98 (n = 7) to 23.98 +/- 2.32 (n = 6) microliters h-1 cm-2 (P < 0.01); polyethylene glycol 4000 permeability was increased from 0.030 +/- 0.001 (n = 7) to 0.047 +/- 0.003 (n = 6) cm/h (P < 0.01) and luminal collagenase activity increased from a negligible control value to 250 +/- 39 (n = 6) units/ml (P < 0.001). Spermine also caused oedema formation within the mucosal interstitial fluid, without inducing an overt breakdown of the mucosa at the luminal surface. 3. Polyamine-free dialysed seminal plasma had no effect on polyethylene glycol 4000 permeability, although it still caused a significant decrease in colonic fluid absorption from 48.83 +/- 2.98 (n = 7) (control) to 31.41 +/- 2.08 (n = 5) microliters h-1 cm-2 (P < 0.01). 4. Low-molecular-mass heparin (600 units/ml) prevented the spermine (5 mmol/l)- and whole-semen-induced increase in colonic polyethylene glycol 4000 permeability and reduced the effect of semen on fluid absorption by 63% (P < 0.001) and that of spermine by 56% (P < 0.01). 5. The Zn2+ chelator and collagenase inhibitor o-phenanthroline reduced the effect of spermine on fluid absorption and polyethylene glycol 4000 permeability by 100% (P < 0.001) and on interstitial oedema formation. o-Phenanthroline also reduced the effects of whole semen on fluid absorption (by 70%, P < 0.01) and on polyethylene glycol 4000 permeability by 95%, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Modulation of endothelial permeability by 1-O-alkylglycerols.

Regulation of endothelial barrier function often occurs through signalling involving phospholipase C activation which produces diacylglycerol (DAG), a lipidic second messenger activator of protein kinase C (PKC). Therefore, modification of lipidic composition of endothelial cell membranes might modify DAG production and, as a result, alter regulation of endothelial permeability. We investigated the in vitro effects of natural 1-O-alkylglycerols on porcine aortic endothelial cell permeability to dye-labelled albumin. [3H]-1-O-alkylglycerols (10 microm) were substantially incorporated into phosphatidylcholine (6.6%) and phosphatidylethanolamine (4.4%). Stimulation of endothelial cell monolayer with phorbol-myristate-acetate or with the calcium ionophore A23187 resulted in a raise in permeability to albumin. Pre-treatment with 1-O-alkylglycerols (10 microm, 24 h) had no effect on basal albumin permeability but totally inhibited the effect of phorbol-myristate-acetate, and brought the permeability of A23187-stimulated endothelial cell monolayers below control. After incubation of cells with [3H]-1-O-alkylglycerols (10 microm, 24 h), we detected the production of the analogue of DAG, and PKC inhibitor, [3H]-1-O-alkyl-2-acyl-glycerol, in resting cells. This production was increased by 58% under A23187 stimulation while phorbol-myristate-acetate had no effect. Our data demonstrate that natural 1-O-alkylglycerols modify endothelial permeability, and suggest that this effect could be mediated through alteration of lipidic signalling.

Albumins↗
PubMed2003

Involvement of enteric nerves in permeability changes due to deoxycholic acid in rat jejunum in vivo.

AIM: Stress and Clostridium difficile toxin A increase epithelial permeability in the small intestine via vagus and visceral afferents, in turn activating mucosal mast cells. Bile acids also increase epithelial permeability but it is not known if nerves or mast cells are involved in this effect in the small intestine. METHOD: In jejunum of anesthetized rats, the effects of hexamethonium and atropine on deoxycholic acid (DCA) induced fluid secretion and increase in epithelial permeability was therefore studied by determining the appearance and disappearance rates of 14C-mannitol and 51Cr-EDTA into and from a perfusion system containing 4 or 8 mm DCA and expressed as clearance. RESULTS: DCA increased net fluid transport and appearance and to a less extent disappearance rates of the probes. Hexamethonium but not atropine, chronic denervation or the NO synthase inhibitor L-NNA did significantly decrease the appearance rate and net fluid secretion. The levels of the mast cell protease II (RMCP II) in perfusate and plasma were not increased by DCA. The clearance ratio Cr-EDTA/mannitol indicates that the plasma clearance of the permeability probes is partly secondary to net fluid transport only at higher DCA concentrations. CONCLUSION: We conclude that the DCA effect on epithelial permeability is to a large part induced by intramural reflex(es) containing nicotinic receptors. The results also suggest that mast cell degranulation and NO release are not involved in the mechanism. This indicates that the nerve effect on intestinal paracellular permeability is not mediated by the mechanisms described for stress or Clostridium difficile toxin A.

Animals↗
PubMed2003

The protective effect of rebamipide on paracellular permeability of rat gastric epithelial cells.

BACKGROUND: Barrier function in gastric epithelial cells is essential for the gastric defence mechanism against acid back-diffusion into the mucosal layer. Our previous study indicated that trans-epithelial resistance (TER) of rat gastric epithelial cells was rapidly increased when the cells were exposed to acid. This response to acid was diminished by indometacin. AIM: Evaluate the effects of a mucoprotective agent, rebamipide, on the nonsteroidal anti-inflammatory drug (NSAID)-induced increase of gastric epithelial permeability. METHODS: Rat gastric epithelial cells were plated on tissue culture inserts. Cells were exposed to a NSAID (indometacin, 10-7 M). Trans-epithelial permeability was measured by TER and diffusion rate of 14C-mannitol. The effect of rebamipide was evaluated by measuring TER. Endogenous prostaglandin E2 (PGE2) production in culture medium was also measured. RESULTS: Indometacin gradually and significantly decreased TER and increased 14C-manitol permeability. Rebamipide reversed the indometacin-induced changes in epithelial permeability and induced PGE2 synthesis. This induction was blocked by either indometacin or a Cyclooxygenase (COX)-2 specific inhibitor. CONCLUSIONS: COX inhibitors such as indometacin inhibit regulation of epithelial permeability by reducing PGE2. COX-1 has an important role in the gastric defense mechanism. Rebamipide suppressed an indometacin-induced increase in gastric epithelial permeability by increasing PGE2 levels in a COX-2 dependent manner.

Alanine↗
PubMed1998

Gastroduodenal permeability in Crohn's disease.

BACKGROUND: Gastric permeability was prospectively investigated by determination of sucrose excretion in 100 patients with Crohn's disease. Results were compared with histological findings and the lactulose-mannitol ratio as a measure of intestinal permeability. METHODS: All subjects underwent oesophagogastroduodenoscopy with biopsies of all investigated parts. Thirty-two Helicobacter pylori-positive patients were excluded from further analyses. RESULTS: Gastroduodenal permeability was significantly higher in patients with Crohn's disease than in control subjects (P < 0.00001). Sucrose excretion alone did not predict microscopic inflammation of the upper gastrointestinal tract. Increased gastroduodenal permeability with a concomitant rise in intestinal permeability predicted histological upper gastrointestinal involvement of Crohn's disease with a likelihood of 86%. The negative predictive value was 43%. CONCLUSION: In parallel with findings in the small intestine, gastroduodenal permeability is increased in a high proportion of patients with Crohn's disease. In patients with an increased lactulose-mannitol ratio, elevated sucrose excretion is highly predictive of histological gastroduodenal involvement.

Adolescent↗
PubMed2003

Increased intestinal permeability as a cause of fluctuating postprandial blood glucose levels in Type 1 diabetic patients.

BACKGROUND: In diabetic patients, postprandial glucose levels, which have a major impact on metabolic control, are determined by the rate of nutrient delivery into the intestine, absorption of nutrients from the small intestine, and the metabolism of the absorbed nutrients by the liver. The present study addresses whether Type 1 diabetic patients have increased intestinal permeability and intestinal permeability predicts postprandial glucose variability. MATERIAL AND METHODS: Thirty Type 1 diabetic patients together with 15 sex- and age-matched healthy controls were enrolled in the study. After an overnight fasting all patients and controls received 100 micro Ci 51Cr of EDTA as a radioactive tracer and the percentage of the isotope excreted in a 24-h urinary specimen was the permeability measure. Instant blood glucose was measured just before the test, and the patients performed and recorded self-monitoring of fasting and 2nd-hour postprandial blood glucose levels during the following week. RESULTS: We found that intestinal permeability is increased in Type 1 diabetic patients compared with age- and sex-matched healthy controls. Increased intestinal permeability is related at least in part to the instant blood glucose level and the presence of diabetic autonomic neuropathy. CONCLUSION: Increased intestinal permeability leads to higher variation in postprandial blood glucose levels, thereby worsening metabolic control.

Blood Glucose↗
PubMed1997

Permeability of dentine after Nd:YAG laser treatment: an in vitro study.

The purpose of this investigation was to determine the effects of Nd:YAG laser treatment on the permeability of dentine. Forty dentine discs were prepared by horizontal sectioning through the middle coronal third of freshly extracted non-carious third molars. After the removal of the pulp the discs were finished with 600 grit and divided into three test groups and one control group (n = 10). For the test group three different laser power settings were chosen: test group A: 3 x 60 sec, 60 mJ; test group B: 3 x 60 sec, 90 mJ; test group C: 3 x 60 sec, 120 mJ. No laser treatment was performed on the control group. In a two-chamber system the filtration rate of dentine tubules from an exactly defined area of the specimens was measured using a radioactive Ringer solution under a pressure of 30 cm H2O. Permeability measurements were carried out three times prior to lasing, three times immediately following laser treatment and six times after the application of phosphoric acid. Analysis of variance showed a significant influence of the Nd:YAG laser treatment on the permeability of dentine (P < 0.001). The mean quotient of non-treated control vs. lased dentine was 2.19 +/- 0.86 for the 60 mJ beam, 1.49 +/- 0.88 for the 90 mJ beam, and 2.04 +/- 2.17 for the 120 mJ beam. Etching the lased surfaces had a statistically significant influence on the permeability of the dentine only in the 60 mJ group (P < 0.001). The data show that the Nd:YAG laser treatment often increases the permeability of smear layer covered dentine but moderates the increase of permeability after etching the surface with phosphoric acid.

Acid Etching, Dental↗
PubMed1998

Glutamate-induced Co2+ uptake in rat auditory brainstem neurons reveals developmental changes in Ca2+ permeability of glutamate receptors.

Ca2+ influx through glutamate receptors (GluRs) is thought to play a crucial part in developmental processes and neuronal plasticity. Here we have examined the spatiotemporal distribution of Ca2+-permeable GluRs in auditory brainstem neurons of the rat from birth to adulthood, using the cobalt-staining technique of Pruss and collaborators. In slices of young adult rats, 1 mM glutamate evoked intense cobalt uptake in subsets of neurons in the ventral cochlear nuclei, the medial nucleus of the trapezoid body, the lateral and the medial superior olive, and the lateral lemniscal nuclei. Neurones in the central nucleus of the inferior colliculus, and thalamic auditory nuclei appear to express few, if any, Ca2+-permeable GluRs. Thus, in adults, Ca2+-permeable GluRs are present in neurons of almost all main relay stations of the auditory brainstem. During development, cobalt-stained cells first appeared at about hearing onset (at postnatal day 12 [P12]). At P16, staining levels were highest and the pattern of distribution was already adult-like. The staining intensity slightly declined during the fourth postnatal week. In contrast, Ca2+-permeable receptors were detected in the external cortex of the inferior colliculus as early as P4. Our results show that auditory neurons, characterized by a high temporal precision in neuronal activity, display Ca2+-permeable GluRs. Because Ca2+ permeability appears at about the onset of hearing and is highest during the following 2 weeks, Ca2+ influx through GluRs is likely to be implicated in remodelling processes occurring during this ontogenetic period.

Animals↗
PubMed1996

Induction of nitric oxide synthase inhibits gap junction permeability in cultured rat astrocytes.

Nitric oxide (.NO) synthase (NOS) was induced in cultured rat astrocytes by incubation with lipopolysaccharide (LPS) for 18 h and gap junction permeability was assessed by the scrape-loading/Lucifer yellow transfer technique. Induction of NOS was confirmed by determining either the NG-methyl-L-arginine (NMMA)-inhibitable production of nitrites and nitrates or the conversion of L-[3H]arginine to L-[3H]citrulline. Incubation with LPS dose-dependently inhibited gap junction permeability to 63.3% at 0.05 microgram/ml LPS and no further inhibition was observed on increasing the LPS concentration up to 0.5 microgram/ml. LPS-mediated gap junction inhibition was irreversible but was prevented by incubation with the NOS inhibitor NMMA and with the superoxide anion (O2.-) scavenger superoxide dismutase. Incubation of the cells with both the .NO donor S-nitroso-N-acetylpenicillamine and the O2.(-)-generating system xanthine/xanthine oxidase inhibited gap junction permeability. These results suggest that the in situ reaction between .NO and O2.-, to form the peroxynitrite anion (ONOO-), may be responsible for the inhibition of gap junction permeability. Scavenging the ONOO- derivative hydroxyl radical (.OH) with either dimethyl sulfoxide or mannitol prevented the LPS-mediated inhibition of gap junction permeability. Finally, exposure of astrocytes to authentic ONOO- caused a dose-dependent inhibition of gap junction permeability (65.7% of inhibition at 0.5 mM ONOO-). The pathophysiological relevance of ONOO(-)-mediated inhibition of gap junctional communication in astrocytes after NOS induction by LPS is discussed, stressing the possible role played by this mechanism in some neurodegenerative diseases.

Animals↗
PubMed2001

Inhibition of nitric oxide synthase reverses changes in peritoneal permeability in a rat model of acute peritonitis.

BACKGROUND: Acute peritonitis is the most frequent complication of peritoneal dialysis (PD), and nitric oxide (NO) is thought to play a role in the structural and permeability changes observed in this condition. We have used a combination of expression, enzymatic and pharmacological studies to substantiate the potential role(s) played by NO during peritonitis. METHODS: The peritoneal equilibration test was performed in control rats and rats with acute peritonitis (originating from skin flora), using standard dialysate supplemented or not with the NO synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME). In parallel, peritoneal NOS enzymatic activities were measured and expression studies for NOS isoforms and S-nitrosocysteine reactivity performed in the peritoneum. RESULTS: In comparison with controls, rats with acute peritonitis were characterized by inflammatory changes, increased S-nitrosocysteine immunoreactivity, and increased NOS activities in the peritoneum, due to the up-regulation of endothelial and inducible NOS. In parallel, rats with acute peritonitis showed increased permeability for small solutes; decreased sodium sieving; loss of ultrafiltration (UF); and increased protein loss in the dialysate. Addition of L-NAME to the dialysate did not induce permeability changes in control rats, but significantly improved UF and reversed permeability modifications in rats with peritonitis. The effect of L-NAME was reflected by a mild but consistent increase in blood pressure during PD exchange. CONCLUSIONS: Our results demonstrate that local generation of NO, secondary to up-regulation of NOS isoforms, plays an important role in the regulation of peritoneal permeability during acute peritonitis in rats. By itself, NOS inhibition improves UF and reverses permeability changes, which might offer new therapeutic perspectives in acute peritonitis.

Acute Disease↗
PubMed1993

[The blood-retina barrier and blood-aqueous humor barrier in type I diabetic patients without retinopathy. Determination of permeability using fluorophotometry and laser flare measurements].

BACKGROUND: Possibly early functional disruption of the blood-ocular barrier in eyes of insulin dependent type I diabetics without manifestation of retinopathy can be detected using fluorophotometry and laser flare measurement. MATERIAL AND METHODS: In order to evaluate blood-retinal (BRB) and blood-aqueous-barrier (BAB) permeability fluorophotometry was performed in 34 eyes of 34 insulin-dependent type-I diabetics without retinopathy, additionally the aqueous laser flare was measured. 34 normal eyes of 34 age-matched subjects served as controls. RESULTS: BRB permeability (3.2 +/- 1.3 x 10(-7) cm/s) was increased with low significance (p = 0.019) in diabetic eyes (controls: 2.6 +/- 0.7). The permeability coefficient of BAB was found to be increased in diabetics (5.3 +/- 1.8 x 10(-4)/cm) with higher significance (controls: 3.7 +/- 0.7; p = 0.00003); laser flare values in diabetic eyes (5.0 +/- 1.2 photon counts/ms) were significantly higher than in controls (4.1 +/- 1.0; p = 0.003). In diabetics there was a significant correlation (r = 0.3; p = 0.014) between the laser flare values and the permeability coefficient of BAB. CONCLUSIONS: In type-I diabetics without retinopathy BRB permeability seems to be increased slightly as well as laser flare in the aqueous; the BAB permeability coefficient seems to be the most sensitive parameter in a beginning affection of the blood-ocular barrier.

Adult↗
PubMed1993

Intestinal permeability is increased after major vascular surgery.

PURPOSE: In experimental animals increased intestinal permeability has been demonstrated after ischemia and reperfusion injury. In this study we determined intestinal permeability in patients after elective or emergency aortic aneurysm repair; the latter patients were in severe shock on hospital admission. METHODS: A dual sugar absorption test, with lactulose and mannitol as markers, was used to measure intestinal permeability on the second day between 24 and 30 hours after hospital admission. RESULTS: The lactulose/mannitol excretion ration was 0.012 +/- 0.005 in seven healthy control subjects, 0.118 +/- 0.116 in seven patients having elective operation, and 0.098 +/- 0.093 in eight patients having emergency operation, indicating a significant increase of intestinal permeability in both patient groups (p < 0.01). No significant difference was found in intestinal permeability between patients of the elective and emergency groups. CONCLUSIONS: A significant increase in intestinal permeability commonly occurs in patients after elective and emergency major vascular surgery. It is suggested that this is mainly due to reperfusion injury rather than the ischemic period of the intestine itself.

Adult↗
PubMed2001

Predominant role of endothelial nitric oxide synthase in vascular endothelial growth factor-induced angiogenesis and vascular permeability.

Nitric oxide (NO) plays a critical role in vascular endothelial growth factor (VEGF)-induced angiogenesis and vascular hyperpermeability. However, the relative contribution of different NO synthase (NOS) isoforms to these processes is not known. Here, we evaluated the relative contributions of endothelial and inducible NOS (eNOS and iNOS, respectively) to angiogenesis and permeability of VEGF-induced angiogenic vessels. The contribution of eNOS was assessed by using an eNOS-deficient mouse, and iNOS contribution was assessed by using a selective inhibitor [l-N(6)-(1-iminoethyl) lysine, l-NIL] and an iNOS-deficient mouse. Angiogenesis was induced by VEGF in type I collagen gels placed in the mouse cranial window. Angiogenesis, vessel diameter, blood flow rate, and vascular permeability were proportional to NO levels measured with microelectrodes: Wild-type (WT) > or = WT with l-NIL or iNOS(-/-) > eNOS(-/-) > or = eNOS(-/-) with l-NIL. The role of NOS in VEGF-induced acute vascular permeability increase in quiescent vessels also was determined by using eNOS- and iNOS-deficient mice. VEGF superfusion significantly increased permeability in both WT and iNOS(-/-) mice but not in eNOS(-/-) mice. These findings suggest that eNOS plays a predominant role in VEGF-induced angiogenesis and vascular permeability. Thus, selective modulation of eNOS activity is a promising strategy for altering angiogenesis and vascular permeability in vivo.

Animals↗
PubMed1981

Proton and hydroxide ion permeability of phospholipid vesicles.

The apparent permeability of H+ through phospholipid bilayers was determined by measuring H+ efflux from large unilamellar phospholipid vesicles with internal space buffered at pH 4. The value obtained is about 10(-9) cm/sec at room temperature, five orders of magnitude lower than was recently reported for the combined permeability for H+ and OH- [Nichols, J. W. & Deamer, D. W. (1980) Proc. Natl. Acad. Sci. USA, 77, 2038-2042]. The apparent permeability measured in this way is the sum of contributions from the movement of H+ and of uncharged species (HCl or HNO3) in equilibrium with anions in the solution. There is evidence that the uncharged species make the dominant contribution and that the permeability coefficient for H+ per se is no larger than 5 X 10(-12) cm/sec. An attempt to measure OH- permeability by use of vesicles buffered at pH 10 did not give a conclusive result because the vesicle walls appeared to be damaged by exposure to this pH. An apparent permeability coefficient of about 10(-7) cm/sec was estimated for undamaged membranes.

Acids↗
PubMed1983

Proton-hydroxide permeability of liposomes.

Liposome permeability to net proton-hydroxide flux was compared under two conditions that have produced extreme values in previous studies. In the first [Nichols, J.W. & Deamer, D.W. (1980) Proc. Natl. Acad. Sci. USA 77, 2038-2042] small pH gradients were permitted to decay near pH 7 and permeability coefficients in the range of 10(-4) cm/sec were obtained. In the second [Nozaki, Y. & Tanford, C. (1981) Proc. Natl. Acad. Sci. USA 78, 4324-4328] the decay rate of large pH gradients (approximately equal to 3 pH units) was measured and apparent permeability coefficients in the range of 10(-9) cm/sec were reported. We have repeated the conditions of the latter study and have found that the decay of large pH gradients produces a diffusion potential that limits net proton-hydroxide flux. The permeability coefficients calculated from the flux are therefore underestimated and do not reflect intrinsic proton permeability. With the same liposome preparations under conditions in which small gradients decay so that diffusion potentials are negligible, the measured permeability coefficient is near 10(-4) cm/sec, as reported earlier.

Anions↗
PubMed1988

Recombinant tumor necrosis factor increases pulmonary vascular permeability independent of neutrophils.

We studied the effects of intravenous infusion of recombinant human tumor necrosis factor type alpha (rTNF-alpha; 12 micrograms/kg) on lung fluid balance in sheep prepared with chronic lung lymph fistulas. The role of neutrophils was examined in sheep made neutropenic with hydroxyurea (200 mg/kg for 4 or 5 days) before receiving rTNF-alpha. Infusion of rTNF-alpha resulted in respiratory distress and 3-fold increases in pulmonary arterial pressure and pulmonary vascular resistance within 15 min, indicating intense pulmonary vasoconstriction. Pulmonary lymph flow (i.e., net transvascular fluid filtration rate) and transvascular protein clearance rate (a measure of vascular permeability to protein) increased 2-fold within 30 min. The increased permeability was associated with leukopenia and neutropenia. The pulmonary hypertension and vasoconstriction subsided but fluid filtration and vascular permeability continued to increase. Sheep made neutropenic had similar increases in pulmonary transvascular fluid filtration and vascular permeability. rTNF-alpha also produced concentration-dependent increases in permeability of 125I-labeled albumin across ovine endothelial cell monolayers in the absence of neutrophils or other inflammatory mediators. The results indicate that rTNF-alpha increases pulmonary vascular permeability to protein by an effect on the endothelium.

Animals↗
PubMed1988

Identification of specific apical membrane polypeptides associated with the antidiuretic hormone-elicited water permeability increase in the toad urinary bladder.

Antidiuretic hormone (ADH) increases the water permeability of the toad urinary bladder. The increase occurs in the apical plasma membrane of granular cells that line the urinary surface of the bladder and is produced by the insertion of water permeability units that have been identified by freeze-fracture electron microscopy as intramembrane particle aggregates. Under water-impermeable conditions, particle aggregates reside in intracellular vesicles called "aggrephores." In response to ADH, the aggrephores fuse with the apical plasma membrane and render it water permeable. When ADH is removed, intramembrane particle aggregates and aggrephores are retrieved from the apical membrane, and it returns to a water-impermeable state. To identify proteins involved in the water permeability response, we used lactoperoxidase/glucose oxidase to 125I-label external apical membrane proteins to compare control and ADH-treated bladders. Several polypeptides were consistently labeled in ADH-treated bladders and not in paired controls. After demonstrating that lactoperoxidase behaves as a fluid-phase marker and is sequestered in aggrephore-like vesicles when ADH is withdrawn, we used the technique of Mellman et al. [Mellman, I.S., Steinman, R. M., Unkeless, J. C. & Cohn, Z. A. (1980) J. Cell Biol. 86, 712-722] to label proteins endocytosed when water permeability declines after ADH is withdrawn to test whether the membrane proteins labeled in ADH-treated bladders behaved like particle aggregates. The internalized membranes contained polypeptides of the same molecular weights (55,000, 17,000-14,000, and 7,000) as those labeled on the apical surface of ADH-treated but not control bladders. These polypeptides are evidently involved in the ADH-stimulated water permeability response and may be components of particle aggregates.

Animals↗