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PubMed1983

Prostaglandin E2, adenosine 3':5'-cyclic monophosphate and changes in endometrial vascular permeability in rat uteri sensitized for the decidual cell reaction.

The possibility that prostaglandin E2 (PGE2) increases endometrial vascular permeability and initiates decidualization in sensitized rat uteri by stimulation of adenosine 3':5'-cyclic monophosphate (cAMP) synthesis was investigated. Immature rats, pretreated so that they were sensitized for the decidual cell reaction, were used. Following the unilateral intrauterine injection of 50 microliters phosphate-buffered saline containing gelatin (PBS-G), a deciduogenic stimulus, uterine concentrations of both PGE and cAMP were elevated as early as 1 min after the intrauterine treatment. To determine if uterine stimuli which increase endometrial vascular permeability also increase uterine cAMP concentrations, rats, treated with or without indomethacin, an inhibitor of PG synthesis, received unilateral intrauterine injections of 50 microliters PBS-G with and without 10 micrograms PGE2 and were killed 15 min later. Uterine cAMP concentrations were elevated in all injected horns except in those of indomethacin-treated rats receiving PBS-G intraluminally, thus paralleling the expected changes in endometrial vascular permeability. As indicated by radioactivity levels in the stimulated horn 15 min after the i.v. injection of 125I-labeled bovine serum albumin, the intrauterine injection of dibutyryl cAMP, with or without theophylline, did not increase endometrial vascular permeability in indomethacin-treated animals. In contrast, cholera toxin, an activator of adenylate cyclase activity, markedly elevated permeability and induced decidualization. Except for the lack of a permeability response to the cAMP analogue, these data are consistent with the hypothesis that the effect of PGE2 on endometrial vascular permeability is mediated by cAMP.

Animals↗
PubMed2005

Purinoceptors are involved in the induction of an osmolyte permeability in malaria-infected and oxidized human erythrocytes.

In human erythrocytes, infection by the malaria parasite Plasmodium falciparum or oxidative stress induces a new organic osmolyte and anion permeability. To examine a role for autocrine purinoceptor signaling during this induction process, erythrocytic purinoceptor expression, and ATP release were determined. Furthermore, using pharmacological and genetic approaches the dependence on purinoceptor signaling of osmolyte permeability and Plasmodium development, both in vitro and in vivo, were assessed. Extracellular ATP did not induce an osmolyte permeability in non-infected or non-oxidized erythrocytes. ATP and other purinoceptor agonists increased the induction of osmolyte permeability during infection or oxidation as measured by isosmotic hemolysis and patch-clamp recording. Purinoceptor antagonists and apyrase decreased the induced permeability. The observed pharmacology suggested the involvement of P2Y purinoceptors. Accordingly, human erythrocytes expressed P2Y1 protein. Moreover, P2Y1-deficient mouse erythrocytes exhibited a delayed appearance of the osmolyte permeability during P. berghei infection- or oxidation compared with wild-type erythrocytes. Furthermore, the nonspecific purinoceptor antagonist suramin decreased in vitro growth and DNA/RNA amplification of P. falciparum in human erythrocytes and decreased in vivo growth of P. berghei. P. berghei developed slower in P2Y1-deficient mice in vivo compared with wild-type animals. In conclusion, induction of the osmolyte permeability in Plasmodium-infected erythrocytes involves autocrine purinoceptor signaling.

Adenosine Triphosphate↗
PubMed2006

Adipose-specific effect of rosiglitazone on vascular permeability and protein kinase C activation: novel mechanism for PPARgamma agonist's effects on edema and weight gain.

PPARgamma agonists, thiazolidinediones, cause fluid retention and edema due to unknown mechanisms. We characterized the effect of rosiglitazone (RSG), a thiazolidinedione, to induce vascular permeability, vascular endothelial growth factor (VEGF) expression, and protein kinase C (PKC) activation with edema and wt gain. In lean, fatty and diabetic Zucker rats, and endothelial insulin receptor knockout mice, RSG increased wt and vascular permeability, selectively in fat and retina, but not in heart or skeletal muscle. H2O content and wt of epididymal fat were increased by RSG and correlated to increases in capillary permeability in fat and body wt. RSG induced VEGF mRNA expression and PKC activation in fat and retina up to 2.5-fold. Ruboxistaurin, a PKCbeta isoform inhibitor, in the latter 2 wk of a 4-wk study, normalized vascular permeability in fat and decreased total wt gain, H2O content, and wt of fat vs. RSG alone but did not decrease VEGF expression, basal permeability, or food intake. Finally, RSG did not increase wt or vascular permeability in PKCbeta knockout vs. control mice. Thus, thiazolidinedione's effects on edema and wt are partially due to an adipose tissue-selective activation of PKC and vascular permeability that may be prevented by PKCbeta inhibition.

Adipose Tissue↗
PubMed1999

Organ preservation solutions increase endothelial permeability and promote loss of junctional proteins.

OBJECTIVE: To investigate the effects of the organ preservation solutions UW and Plegisol on endothelial permeability; occludin and vascular endothelial (VE)-cadherin content in human umbilical vein endothelial cells (HUVEC); and junctional localization of these proteins after exposure to these solutions. SUMMARY BACKGROUND DATA: Organ preservation for transplantation is limited by several challenges, including loss of tissue function, tissue injury, and tissue edema. Occludin and VE-cadherin are responsible for maintaining and regulating the endothelial solute barrier. Several studies have noted organ edema and dysfunction with preservation, as well as gaps between endothelial cells suggesting that disorganization of junctional proteins (e.g., occludin and VE-cadherin) is responsible for interstitial edema. METHODS: HUVEC monolayers were treated with 4 degrees C UW and Plegisol for 3 and 6 hours and then reperfused with normal buffer. Permeability was examined using FITC-dextran tracer during the reperfusion phase. Occludin and VE-cadherin content at different time points was measured by Western blotting. Treated groups were also examined by immunofluorescence for occludin, VE-cadherin, and F-actin. RESULTS: Compared with untreated controls, cold preservation for 3 and 6 hours increased endothelial permeability after rewarming, which appears to depend on the duration of cold exposure. Monolayers exposed to 3 hours of cold preservation did not have increased permeability in the first hour after rewarming but had significantly increased permeability after the first hour and all subsequent time points. Monolayers exposed to 6 hours of cold preservation had increased permeability after the first hour and at all later time points. Western blotting demonstrated that occludin content was decreased to a similar extent with all solutions after 3 hours of cold preservation. Six hours of cold preservation in Plegisol reduced the occludin content significantly compared with UW and control. VE-cadherin content was unchanged after 3 hours of cold preservation but was dramatically reduced in all groups at 6 hours. Immunofluorescent staining demonstrated junctional gap formation and discontinuous staining of occludin and VE-cadherin with all cold preservation protocols; changes in F-actin organization were observed at 3 and 6 hours after cold preservation. CONCLUSION: The changes in occludin, VE-cadherin, and F-actin content and organization and increased permeability associated with cold storage demonstrate that alterations of the tight and adherens junctions may underlie organ edema associated with cold organ preservation. These data also suggest that novel strategies to maintain the content and integrity of endothelial junctional proteins may provide an important therapeutic avenue for organ preservation.

Adenosine↗
PubMed1995

Effects of malignancy and interleukin-2 infusion on gut macromolecular permeability.

OBJECTIVE: Enhanced gut permeability has been shown in patients with advanced malignancy. The dramatic inflammatory shock syndrome produced by high-dose interleukin-2 immune therapy could further change gut barrier function. This study measured the effect of advanced renal cell carcinoma and malignant melanoma, and interleukin-2 treatment on gut permeability. DESIGN: Nonrandomized, controlled study. SETTING: University hospital. PATIENTS: Adults with metastatic, unresectable renal cell carcinoma or metastatic, malignant melanoma, and normal volunteers. INTERVENTIONS: Gut permeability was measured in patients with renal cell carcinoma or malignant melanoma before and during interleukin-2 infusions, using polyethylene glycol 3350 and polyethylene glycol 400. The polyethylene glycols were administered orally within 48 hrs of interleukin-2 therapy and the 24-hr urine excretions were measured. MEASUREMENTS AND MAIN RESULTS: Increased permeability was seen in the baseline state of these patients (ratio of polyethylene glycol 3350 to polyethylene glycol 400 = 1.1 +/- 0.7 x 10(-2)) when compared with normal volunteers (ratio = 0.48 +/- 0.2 x 10(-2); p < .05). However, after interleukin-2 treatment, no further increase in permeability was seen (ratio = 1.4 +/- 0.8 x 10(-2)). CONCLUSIONS: Gut permeability to polyethylene glycol 3350 is enhanced in advanced malignancy. High-dose interleukin-2 therapy does not further increase permeability of the gut.

Adult↗
PubMed1999

In vitro evaluation of vascular permeability to contrast media using cultured endothelial cell monolayers.

OBJECTIVE: The efficiency of contrast agents in medical imaging depends on their distribution into vascular and interstitial compartments. The aim of this study was to compare in vitro endothelial permeability to different classes of contrast agents with various vascular persistence properties: a triiodinated nonionic monomer (ioversol), an iodinated dextran polymer (P604), and an iron oxide nanoparticle (sinerem). METHODS: Permeability studies, through collagen-coated filters with or without porcine aortic endothelial cell monolayer, were carried out by placing each filter-ring (luminal chamber) into a beaker containing a culture medium (abluminal chamber). Contrast media, diluted in the culture medium, were added to the luminal chamber. Aliquots were sampled from the abluminal chamber for contrast agent determinations. The volume cleared of the compound was calculated from the luminal side to the abluminal side. Parallel permeability tests to [3H]-H2O and Evans blue albumin were performed as references. Finally, the modulatory effect of bradykinin on endothelial permeability to albumin or to contrast agents was studied. RESULTS: The volume cleared of ioversol, P604, and sinerem through membrane filters was decreased by 19.6%, 32.1%, and 52.0%, respectively, in the presence of a cell monolayer. Bradykinin (10(-6) M) significantly increased permeability to albumin, ioversol, and sinerem. Ioversol and sinerem induced a significant decrease in permeability to albumin. CONCLUSIONS: A relation between the molecular size of the contrast agents tested and their endothelial permeability can be established with this in vitro model.

Analysis of Variance↗
PubMed2001

Basal release of nitric oxide and its interaction with endothelin-1 on single vessel hydraulic permeability.

BACKGROUND: Both endothelin-1 (ET-1) and nitric oxide (NO) are released by the endothelium and are implicated in modulating the permeability of the endothelial barrier. The present study was designed to examine the interaction between ET-1 and NO and its influence on microvascular permeability as well as the role of NO in maintaining microvascular permeability. To isolate the direct effect of ET-1 and NO, experiments were conducted under conditions where hydraulic and oncotic pressures were controlled. METHODS: Postcapillary venules in the rat mesentery were perfused in situ and paired measurements of hydraulic permeability (Lp) obtained using the modified Landis micro-occlusion method. The effect of basal endogenous NO was tested by measuring the effects of perfusion with the NO synthase inhibitor Nw-nitro-L-arginine-methyl-ester (L-NAME) (100 micromol/L) on Lp (n = 6). In addition, Lp measured after a 15-minute perfusion with L-NAME (100 micromol/L) was compared with measures of Lp obtained after perfusion with a combined mixture of L-NAME (100 micromol/L) and ET-1 (80 pmol/L) (n = 6). RESULTS: Units for Lp are mean +/- SE x 10(-8) cm x sec(-1) x cm H2O(-1). Under basal conditions, in the absence of exogenous ET-1, NO synthase inhibition led to a significant increase in Lp from 5.7 +/- 0.5 to 9.8 +/- 1.4 (p = 0.02). Compared with L-NAME alone, ET-1 + L-NAME significantly decreased Lp from 10.3 +/- 0.8 to 5.7 +/- 0.6 (p = 0.006). CONCLUSION: Constitutive release of NO from the microvascular endothelium plays a role in maintaining a basal level of microvascular permeability. Decreases in microvascular permeability seen with the administration of ET-1 are not mediated via the release of NO. These findings suggest important roles for ET-1 and NO in maintaining and modulating microvascular permeability.

Animals↗
PubMed1997

Nonhomogeneous permeability of canine anulus fibrosus.

STUDY DESIGN: This report examines the permeability coefficient and aggregate modulus of slices of anulus cut from canine lumbar intervertebral discs. OBJECTIVES: To examine the influence of radial position on the properties of these materials, including outer samples with intact anulus edge. SUMMARY OF BACKGROUND DATA: The outer edge of anulus fibrosus shows radial bulge during axial compression of motion segments. The radial bulge increases monotonically when the axial compression is sustained for several hours, until a plateau is reached. Triphasic modeling of axial compression shows that this time course of radial bulge can not be obtained using a uniform permeability coefficient according to values in the literature. METHODS: Confined consolidation experiments (controlled load) were designed to measure the time course of uniaxial deformation of samples of anulus that were 4 mm in diameter and 1 mm tall. The rotation symmetry axis of the samples was defined in the radial direction of the disc. The radial permeability coefficient and the aggregate modulus were determined using the consolidation data and the linear biphasic theory. RESULTS: The permeability coefficient was lower at the periphery than in deeper layers of the anulus. Outer samples with outer surfaces that were 0.0-0.5 mm from the anulus edge had an average permeability coefficient of (1.02 +/- 0.57) x 10(-16) m4/Ns (n = 24). Inner samples that were 2.0-2.5 mm from the anulus edge had an average permeability coefficient of (2.81 +/- 0.98) x 10(-16) m4/Ns (n = 13). The aggregate modulus HA of outer samples was significantly higher (HA = 1.56 +/- 0.34 MPa) than that of inner samples (HA = 1.31 +/- 0.47 MPa). CONCLUSIONS: The fact that the outer anulus is less permeable than the inner anulus may explain why radial bulge of anulus fibrosus increases monotonically in time to an equilibrium value during sustained axial compression of a motion segment.

Animals↗
PubMed1999

Intestinal permeability in liver cirrhosis.

OBJECTIVE: To determine the changes in intestinal permeability in liver cirrhosis and to investigate whether intestinal permeability relates to the stage and aetiology of cirrhosis or existence of spontaneous bacterial peritonitis (SBP). DESIGN: A prospective study of intestinal permeability in patients with cirrhosis. SETTING: Gastroenterology and Nuclear Medicine Departments of Ege University Hospital. PARTICIPANTS: Intestinal permeability was assessed in 44 consecutive patients with cirrhosis and 10 healthy volunteers by measuring 24 h urine excretion of (99m)technetium diethyl triamine penta-acetic acid (99mTc DTPA). Cases with an associated disease, impaired renal function, continuing alcohol consumption and drug intake which is known to have an effect on intestinal permeability were excluded. MAIN OUTCOME MEASURES: Comparisons of 24 h urine excretion of 99mTc DTPA were made between the groups of cirrhotics and controls, different grades of cirrhosis (according to Child-Pugh criteria), alcoholic and non-alcoholic cirrhotics and cirrhotic patients with and without SBP. RESULTS: Patients with cirrhosis excreted 99mTc DTPA significantly more than controls (11.56 +/- 8.96% in cirrhotics and 4.30 +/- 1.49% in controls, P < 0.0001). There was no relationship of 24 h urine excretion of the tracer with the grade and aetiology of cirrhosis (12.20 +/- 9.47%, 11.41 +/- 9.84%, and 11.09 +/- 8.42%, in Child A, B, and C groups and 8.45 +/- 6.57% and 12.05 +/- 9.25% in alcoholic and non-alcoholic cirrhotics, respectively). No significant difference was found between cirrhotic patients with and without SBP in terms of excretion of the administered dose of 99mTc DTPA (9.98 +/- 9.47% and 12.20 +/- 8.82%, respectively). CONCLUSIONS: This study shows that intestinal permeability increased in cirrhotic patients regardless of the grade and aetiology of disease. The presence of SBP does not seem to be due to increased intestinal permeability.

Bacterial Infections↗
PubMed2004

Modulation of microvascular hydraulic permeability by platelet-activating factor.

BACKGROUND: Platelet-activating factor (PAF) is a modulator of the inflammatory response to shock. Edema formation and intravascular fluid loss have been associated with PAF. The increase in microvessel permeability caused by PAF may be related to direct endothelial cell activation and leukocyte activation. We hypothesized that PAF increases hydraulic permeability by means of the direct activation of endothelial cells. METHODS: Hydraulic permeability (Lp) was measured in rat mesenteric venules using the modified Landis micro-occlusion technique. After baseline Lp measurements, paired measures of Lp were obtained during PAF perfusion at doses of 0.1 nmol/L (n = 6), 1.0 nmol/L (n = 6), 10 nmol/L (n = 6), and 50 nmol/L (n = 6). The temporal effects of pulse administration of PAF and repeated exposures to PAF were also assessed. RESULTS: Compared with baseline values (Lp = 1.16 +/- 0.11), the Lp of the microvessels significantly increased at PAF doses of 0.1 nmol/L (Lp = 1.46 +/- 0.1) (p < 0.002), 1 nmol/L (Lp = 2.0 +/- 0.11) (p < 0.004), 10 nmol/L (Lp = 4.09 +/- 0.09) (p < 0.005), and 50 nmol/L (Lp = 5.13 +/- 0.07) (p < 0.0001). All units for Lp are given as +/- SE x 10 -7 cm s-1. cm H2O-1. CONCLUSION: PAF increased microvessel permeability in a dose-dependent manner. The permeability-increasing effect of PAF was transient even with continuous endothelial exposure to PAF. This study emphasizes the ability of PAF to directly modulate microvascular permeability and increase venular permeability.

Animals↗
PubMed1991

Vascular permeability enhancement by Vibrio mimicus protease and the mechanisms of action.

Vibrio mimicus, a causative agent of gastroenteritis, has also been reported to attribute to extraintestinal infections. Recently we have purified a metalloprotease produced by the pathogen: however, the role of the protease in V. mimicus infection has not been documented. The V. mimicus protease (VMP) was found to enhance vascular permeability and form edema when injected into the dorsal skin of guinea pig and rat. The permeability enhancement by VMP was observed in a dose-dependent manner in both guinea pig and rat skin. In guinea pig, an inhibitor of the angiotensin-converting enzyme was found to augment the permeability enhancement reaction. The permeability enhancement was significantly blocked by soybean trypsin inhibitor (SBTI), an inhibitor of plasma kallikrein reaction. In vitro conversion of plasma prekallikrein to kallikrein by VMP was also noted. In rat skin, the permeability enhancement reaction was not blocked by antihistamine or SBTI. However, the reaction was partially blocked when a mixture of antihistamine and SBTI was administered with VMP. It is apparent from the study that in guinea pig skin, VMP enhances vascular permeability through activation of plasma kallikrein-kinin system which generates bradykinin, whereas in addition to the activation of plasma kallikrein-kinin cascade in the case of rat, stimulation of histamine release from mast cells and other unknown mechanism seem to be also a cause of the permeability enhancement reaction. These results suggest that VMP may play a role in extraintestinal infections with edema caused by the pathogen.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2004

Interleukin-4 increases the permeability of human endothelial cells in culture.

BACKGROUND: IL-4 plays a key role in the induction of allergic inflammation, but its role as an effector molecule is less well-established. Although some observations suggest that IL-4 may mediate increased vascular permeability, which is a characteristic feature of allergic inflammation, evidence for a direct effect on endothelial cell permeability is lacking. OBJECTIVE: To determine the effect of human IL-4 on the albumin permeability of cultured human endothelial cells. METHODS: Human umbilical vein endothelial cells were cultured on permeable membranes and the albumin permeability of endothelial monolayers was measured with and without exposure to recombinant human IL-4. Endothelial cells were exposed to various concentrations of IL-4 (0.001-100 U/mL), for various durations (6-24 h), either in the presence or absence of anti-IL-4 antibody. Recovery of endothelial barrier function following exposure to IL-4 was also examined. RESULTS: IL-4 induced a dose-dependent, reversible increase in endothelial permeability to albumin. Low concentrations of IL-4 (1 U/mL) induced a significant increase in endothelial permeability (P=0.004). IL-4-mediated endothelial leak occurred rapidly, within 6 h of exposure. CONCLUSIONS: IL-4 has the capacity to induce vascular leak by a direct effect on cultured endothelial cells, suggesting a potential effector role for IL-4 in the pathogenesis of vascular leak in allergic diseases.

Capillary Permeability↗
PubMed2005

A case-control study of bronchial asthma associated with ulcerative colitis: role of airway microvascular permeability.

BACKGROUND: Recent attention has been devoted to the respiratory manifestations that may be associated with diseases of distant organs. The most prevalent and distinctive pattern of respiratory involvement in ulcerative colitis (UC) is airway inflammation. OBJECTIVE: This study was designed to examine the contribution of airway microvascular permeability to the pathophysiological association of asthma with UC. METHODS: Sputum induction and methacholine provocation test were performed in 27 asthmatic patients (15 without UC and 12 with UC), nine patients with UC and 15 normal controls. Inflammatory indexes, vascular endothelial growth factor (VEGF) levels in induced sputum, airway vascular permeability index and exhaled nitric oxide (NO) levels were examined in all subjects. RESULTS: The percentage of eosinophils and concentration of eosinophil cationic protein in induced sputum were similar in all four groups. Though exhaled NO levels were significantly higher in asthmatics with or without UC than in normal controls or UC patients, these levels were comparable in asthmatics with and without UC. VEGF levels in induced sputum and airway vascular permeability index were significantly higher in asthmatics without UC (VEGF: 1920 (990) pg/mL; airway vascular permeability index: 0.018 (0.008)) and asthmatics with UC (6570 (1000) pg/mL; 0.040 (0.006)) than in normal controls (950 (700) pg/mL; 0.009 (0.003)), whose levels were comparable to those of UC patients (900 (600) pg/mL; 0.011 (0.003)). In particular, these parameters were markedly increased in asthmatics with UC than in asthmatics without UC. VEGF level was significantly correlated with airway vascular permeability index in asthmatics with UC. Moreover, VEGF level and airway vascular permeability index was inversely correlated with degree of airway obstruction and airway hyper-reactivity to methacholine in these asthmatics. CONCLUSION: Airway microvascular hyper-permeability induced by VEGF may have a profound effect on airway function and can explain the heightened airway hyper-responsiveness characteristic of asthma associated with UC.

Adult↗
PubMed1995

Ion permeability of the cytoplasmic membrane limits the maximum growth temperature of bacteria and archaea.

Protons and sodium ions are the most commonly used coupling ions in energy transduction in bacteria and archaea. At their growth temperature, the permeability of the cytoplasmic membrane of thermophilic bacteria to protons is high compared with that of sodium ions. In some thermophiles, sodium is the sole energy-coupling ion. To test whether sodium is the preferred coupling ion at high temperatures, the proton- and sodium permeability was determined in liposomes prepared from lipids isolated from various bacterial and archaeal species that differ in their optimal growth temperature. The proton permeability increased with the temperature and was comparable for most species at their respective growth temperatures. Liposomes of thermophilic bacteria are an exception in the sense that the proton permeability is already high at the growth temperature. In all liposomes, the sodium permeability was lower than the proton permeability and increased with the temperature. The results suggest that the proton permeability of the cytoplasmic membrane is an important parameter in determining the maximum growth temperature.

Archaea↗
PubMedDate not supplied

The effects of sodium chloride, urea and mannitol on the permeability in vitro fo rat papillary collecting ducts to THO, 14C-urea and 22Na.

1. The diffusional permeabilities of collecting duct membranes to THO, 14C-urea and 22Na+ have been measured at different concentrations of urea, NaCl and mannitol. 2. In the absence of urea in perfusate and bath or in its presence in low concentrations, the diffusional permeability to urea was 2.0 (s.e.m. = 0.15, n = 58) micrometer s-1, compared with 0.87 (s.e.m. = 0.06, n = 29) microgram s-1 when 200 mmol/l urea was present. The permeability of the collecting ducts to THO or Na+ was not affected by the different urea concentrations. 3. High concentrations of sodium chloride increased the diffusional permeability of collecting ducts to water and urea but did not affect the diffusional permeability of the collecting duct to Na+. 4. Mannitol had effects similar to those of sodium chloride. 5. In all media tested there was an increase in THO and urea permeability when supramaximal amounts of antidiuretic hormone were added. The increases in the various media for each substance were similar, despite widely different starting permeabilities. 6. The results suggest that solutes and water move across collecting duct epithelium by several pathways that respond differently to various stimuli.

Animals↗
PubMedDate not supplied

The permeability of collecting ducts to 22Na+ and 36Cl- in rat isolated papillae.

1. The diffusional permeability of collecting ducts to 22Na+ and 36Cl- was measured in rat papillae in vitro. 2. The permeability of the collecting duct to 36Cl- was 0.72 (s.e.m. = 0.01; n = 356) microns/sec which was significantly higher than the value of 0.51 (s.e.m. = 0.01; n = 356) microns/sec measured for 22Na+. 3. Collecting ducts in papillae taken from rats on a high sodium intake had a 22Na+ permeability of 0.63 (s.e.m. = 0.04; n = 53) microns/sec which was significantly higher than the value on a normal salt intake (0.50, s.e.m. = 0.04; n = 46 microns/sec). 4. When papillae from normal rats were studied in plasma taken from salt loaded rats, the 22Na+ permeability of 0.59 (s.e.m. = 0.04; n = 18) microns/sec was significantly higher than when incubated in plasma from normal rats (0.44, s.e.m. = 0.05; n = 12) microns/sec. 5. An extract of urine with natriuretic activity had no effect on 22Na+ permeability when tested in this system. 6. Adrenalectomy, PGE2, indomethacin and antidiuretic hormone had no significant effect on 22Na+ and 36Cl- permeability. 7. A substance exists in plasma from salt loaded animals that increases the permeability of collecting ducts to sodium. This effect could explain the component of the natriuresis that follows saline infusion which is independent of changes in glomerular filtration rate, aldosterone, or proximal tubule reabsorption.

Animals↗
PubMedDate not supplied

Uric acid permeability coefficient in the rat papillary collecting duct.

1. While it is believed that the mammalian distal nephron is not involved in uric acid transport, this has not been directly evaluated. Nevertheless, some studies are consistent with significant distal nephron transport. 2. As uric acid transport in man may be similar to the rat, undirectional uric acid permeability was evaluated by perfusion of the isolated rat papillary collecting duct. 3. Uric acid permeability was 0.61 +/- 0.04 micron/s, which was similar to sodium permeability (0.66 +/- 0.05 micron/s) but was less than chloride permeability (0.93 +/- 0.07 micron/s) and markedly less than water permeability (4.81 +/- 0.21 micron/s). Uric acid permeability was not changed following the addition of a maximal antidiuretic concentration of arginine vasopressin (200 microU/mL), nor was it changed by altering the uric acid concentration in the perfusate and bath. 4. These results demonstrate that the papillary collecting duct is permeable to uric acid. The coefficient of transport is sufficiently low and insensitive to arginine vasopressin and uric acid concentrations to suggest that any transport that occurs is probably passive and only of minor physiological significance.

Animals↗
PubMed1997

Protein kinase inhibitor attenuates an increase in endothelial monolayer permeability induced by tumour necrosis factor-alpha.

We questioned the mechanism of the increase in pulmonary endothelial permeability induced by tumour necrosis factor-alpha (TNF-alpha), a cytokine implicated in the pathogenesis of adult respiratory distress syndrome. As a measure of permeability, we determined the albumin transferred across cultured pulmonary endothelial monolayers prepared on a porous filter. The agents evaluated included protein kinase inhibitors H-7 and H-8, a calmodulin antagonist W-7, and protein kinase C (PKC) activators, phorbol myristate acetate (PMA) and SC-9. H-7, more potent in inhibiting PKC than H-8, failed to attenuate the increase in permeability induced by TNF-alpha. Neither PMA nor SC-9 increased permeability. However, H-8, which is a potent inhibitor of cyclic nucleotide-dependent protein kinases, prevented the increase in permeability induced by TNF-alpha. These results suggest that protein kinase other than PKC are involved in the signal transduction in endothelial permeability increase induced by TNF-alpha. Calmodulin pathway may not be implicated in the increase in permeability induced by TNF-alpha.

Albumins↗