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Biomedical subjects

D Erlij

Publications and source records attributed to D Erlij.

At least 73 records · Page 4Linked to original sources
PubMed1973

Sodium uptake by frog skin and its modification by inhibitors of transepithelial sodium transport.

1. The suitability of inulin and mannitol as markers of the diffusional space that exists between the surface of frog skin and the outer barrier to sodium transport has been compared in experiments designed to measure the rapid uptake of sodium.2. Inulin and mannitol both equilibrate finally with the same space at the outer surface of the frog skin, but the rate at which this equilibration occurs is considerably faster for mannitol.3. The dependence of the rapid uptake of sodium on the concentration of sodium in the external medium, using mannitol to correct for extracellular sodium, can be described by simple saturation kinetics with an apparent K(m) for sodium entry of 24 mM and a maximal rate of uptake of 1.28 muequiv/cm(2). hr.4. The effect of amiloride is to inhibit sodium uptake, the degree of inhibition depending both on the concentration of sodium in the external medium and on the level of transepithelial transport normally maintained by the skin.5. Ouabain inhibits sodium uptake when the tissue has been pre-incubated in sodium containing medium. It has no effect on sodium uptake if the pre-incubation takes place in sodium free medium.6. A short-circuit current and potential difference can be elicited across frog skin in the presence of ouabain, by increasing the concentration of sodium bathing the outside surface. This potential and short-circuit current is abolished by the presence of amiloride.7. These results provide direct evidence that amiloride acts to stop entry of sodium into the transport compartment and suggest that the ouabain inhibition of sodium uptake is mediated primarily through an increase of epithelial sodium concentration.

Amiloride↗
PubMed1972

Permeable junctional complexes. The movement of lanthanum across rabbit gallbladder and intestine.

Ionic lanthanum has been used to study transepithelial ion permeation in in vitro rabbit gallbladder and intestine (ileum) by adding 1 mM La(3+) to only the mucosal bathing solution. Transepithelial fluid transport electrical potential differences (p.d.), and resistances were measured. During La(3+) treatment the gallbladder's rate of active solute-coupled fluid transport remained constant, the resistance increased, and the 2:1 NaCl diffusion p.d. decreased. Mucosa-to-serosa fluxes of (140)La(3+) were measured and indicate a finite permeability of the gallbladder to La(3+). La(3+) also increased the transepithelial resistance and p d. of ileum. Electron microscopic examination of La(3+)-treated gallbladder showed: (a) good preservation of the fine structure, (b) electron-opaque lanthanum precipitates in almost every lateral intercellular space, most frequently near the apical end of the lateral spaces close to or within the junctional complex, (c) lanthanum among the subjacent muscle and connective tissue layers, and (d) lanthanum filling almost the entire length of so-called "tight" junctions. No observations were made which unequivocally showed the penetration of lanthanum into the gallbladder cells. Electron micrographs of similar La(3+)-treated ilea showed lanthanum deposits penetrating the junctional complexes. These results coupled with other physiological studies indicate that the low resistance pathway for transepithelial ion permeation in gallbladder and ileum is through the tight junctions A division of salt-transporting epithelia into two main groups, those with "leaky" junctional complexes and those with tight junctional complexes, has been proposed.

Animals↗
PubMed1971

Localization of permeability barriers in the frog skin epithelium.

Ruthenium red and colloidal lanthanum were used to determine the site of the structural barriers to diffusion within the intercellular spaces of frog skin epithelium. Electron micrographs show that occluding zonules located at the outer border of the stratum corneum and at the outer layer of the stratum granulosum are true tight junctions since they are impermeable to these tracers. Measurement of (140)La uptake by the living skin shows that lanthanum moves across the external surface of the skin readily, into and out of a compartment that has a limited capacity and is bounded on its internal side by a barrier impermeable to lanthanum. Examination of these skins with the electron microscope suggests that the compartment is localized between the external membrane of the cells at the outer layer of the s. granulosum and at the outermost surface of the skin. These observations and other findings described in the literature indicate that the site of the external high resistance barrier of the frog skin is localized at the outer border of the s. granulosum.

Absorption↗
PubMed1971

Sodium transport across the isolated epithelium of the frog skin.

1. A method to separate the epithelium from the underlying layers of the frog skin is described. The method is based on the combined use of collagenase and hydrostatic pressures.2. The potential difference and the short-circuit current values of isolated epithelia and whole skins are similar. Na net flux and short-circuit current are equivalent.3. The time course of changes in potential following rapid changes in composition of the bathing solutions shows that the barrier to K diffusion at the internal surface of the isolated epithelium is larger than the barrier to Na diffusion at the external surface.4. In the isolated epithelium there are 133 m-mole K(+) and 24.7 m-mole Na/l. cellular water. The amount of extracellular water was considered to be equal to the inulin space.5. Arginine vasopressin (0.1 u./ml.) markedly increased short-circuit current and potential difference in isolated epithelia. The amount of Na in the epithelium that equilibrated with Na in the external solution was not increased by the hormone.6. Ouabain (10(-4)M) reduced short circuit current and potential difference to values close to zero. The ouabain treated epithelia contained an increased amount of Na originating in the internal solution. On the other hand the amount of Na that originated from the external solution was not increased.7. The amount of epithelial Na that equilibrated with Na in the external solution was 0.009 mu-equiv/cm(2). This figure is about ten times smaller than the values found in whole skins.

Animals↗
PubMed1971

The effects of ethacrynic acid and other sulphydryl reagents on sodium fluxes in frog muscle.

1. Ethacrynic acid (2 mM) increased the sodium efflux from freshly dissected frog sartorius muscles. This increase was not observed in muscles previously treated with strophanthidin.2. In strophanthidin-treated muscles, the addition of ethacrynic acid (2 mM) caused a reduction of sodium efflux. The value of efflux reached in these muscles is similar to that observed in muscles immersed in sodium-free solutions containing strophanthidin.3. Ethacrynic acid reduced sodium influx into strophanthidin-treated muscles. Potassium influx was not affected by this substance. These findings suggest that the inhibitor blocks an exchange of sodium for sodium.4. The increase in sodium efflux caused by ethacrynic acid did not result from depolarization nor from an increase in [Na](i).5. Ethacrynic acid caused only a reduction of sodium efflux in muscles previously loaded with sodium by prolonged immersion in potassium-free solutions at low temperatures.6. A derivative of ethacrynic acid that lacks the ability to combine with sulphydryl (SH) groups did not reduce sodium efflux from muscles treated with strophanthidin.7. Para-chloromercuribenzoic acid (PCMB) reduced sodium efflux from control and strophanthidin-treated muscles. This reduction seems to be restricted to the sodium dependent component of the efflux.8. The inhibition of the sodium-dependent component of sodium efflux caused by ethacrynic acid and PCMB appears to have a similar mechanism, namely, the combination with SH groups.

Animals↗
PubMed1970

The mechanism of the paralysing action of tetramisole on Ascaris somatic muscle.

1. Tetramisole (100 mug/ml) paralysed live Ascaris in 3 min.2. Tetramisole (10 mug/ml) caused a sustained contraction of the isolated somatic muscles of the worm. This contraction was not blocked by curare nor by piperazine.3. Tetramisole reduced the resting potential of Ascaris muscle from 34+/-4 to 10+/-1 mV.4. Tetramisole caused contraction of Ascaris muscle previously depolarized with high K(+) solutions. This observation suggests that tetramisole can induce a contracture that is independent of membrane depolarization.

Acetylcholine↗