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Biomedical subjects

C Lippe

Publications and source records attributed to C Lippe.

At least 55 records · Page 3Linked to original sources

[Uptake of L-(+)lactate by cell membrane (luminal and contraluminal) isolated from rat small intestine microvilli].

L-lactate uptake was measured in vesicles formed by intestinal brush border and baso-lateral membranes, using a rapid filtration technique. In the presence of a Na+ gradient directed into the vesicle, L-lactate can be transiently accumulated in brush border vesicles, but not in baso-lateral ones. The transient L-lactate accumulation does not occur in the presence of a KCl gradient. alpha-cyanocinammic acid strongly inhibits L-lactate uptake in brush border vesicles, but not in baso-lateral ones. These results support the existence of a carrier mediated, Na+ dependent, transport of L-lactate across the brush border membrane.

Animals↗

Colchicine effect on the permeability of the whole epithelium and of isolated cells of frog skin.

The effect of 2 X 10(-5) M colchicine on epithelial cells isolated from frog skins was investigated. Three hours of treatment with colchicine did not change either Na+ and K+ content of isolated cells or nonelectrolyte permeability. When ADH (50 mU/ml) was added, thiourea uptake values became greater than without the hormone; the same values were found in the cells previously treated with colchicine. Na+ transepithelial transport, measured by means of short-circuit current, was inhibited by the antimitotic agent both under control conditions and after ADH stimulation. These results support the view that colchicine does not directly affect ADH action on membrane permeability, but influences some mechanism that controls ADH action on transepithelial transport. Intercellular junctions appear to be the location of such a mechanism.

Animals↗

Colchicine inhibition of ADH effect on frog skin permeability.

ADH and AMPc enhance both thiourea unidirectional fluxes in frog skin. This effect is completely abolished by colchicine pretreatment. The ADH increase of thiourea discharge with or without colchicine led us to suppose that colchicine does not directly affect ADH action on outer membrane permeability, but exerts its effects on a site which is limiting for the ADH action on transepithelial permeability.

Animals↗

Facilitated transport of urea across the gall-bladder luminal membrane.

Counterflow experiments demonstrate the existence of urea counter-transport on the epithelium luminal surface. This phenomenon disappears when 10(-4) M phloretin is added to the perfusion fluid. Moreover counterflow experiments made using thiourea as elicitor, demonstrate that the phenomenon is specific for the urea.

Animals↗

Noradrenaline induced secretion of nonelectrolytes through frog skin.

Addition of noradrenaline (4 x 10(-5) M) to the inner bathing fluid in the skin of the frog Rana esculenta results in increased unidirectional fluxes of urea, thiourea, N-methyl-thiourea, N-N'-dimethylthiourea and mannitol. Fluxes towards the external medium (phi o) undergo a much greater increase than those moving the opposite direction (phi i). The effect of noradrenaline on phi o is higher for urea and thiourea than mannitol, while its effect on phi o thiourea derivatives is related to lipid solubility. This phenomenon does not occur for phi i of the same molecules. FCCP (10(-6) M) pretreatment strongly inhibits the noradrenaline effect on phi o. In skin pretreated with colchicine (2 x 10(-5) M) both urea fluxes are increased to the same extent by noradrenaline. Noradrenaline is concluded to exert two separate effects: (1) a change in permeability in both directions; (2) a secretion of nonelectrolytes towards the external fluid. Such secretion is most probably associated with the hormone-induced secretion of fluid and electrolytes, perhaps mediated by an exocytotic mechanism.

Animals↗

Facilitated transport of urea across the toad gallbladder.

The toad gallbladder epithelium is much more selective than that of the rabbit especially as to the permeability of two molecules like urea and thiourea. These observations can probably be attributed to different permeation mechanisms of the 2 molecules. Neither active transport nor solvent drag can explain these phenomena. 10(-4) M phloretin strongly inhibits urea movement, but does not alter either thiourea fluxes or isotonic net water transport: these results suggest that a specific mechanism is involved in urea movement. The urea transport shows saturation kinetic which is consistent with the presence of a facilitated mechanism.

Animals↗

Permeability pathways for non-electrolytes through Bufo bufo gall-bladder.

Amphotericin B treatment increases the thiourea, D-xylose and mannitol fluxes and lowers those of urea, N-methyl-urea, acetamide, formamide, and N-N'-dimethyl-thiourea. The degree of flux inhibition is related to the cellular permeability of these compounds. Most probably Amphotericin B increases the permeability of all those molecules across the luminal plasma membrane, but simultaneously elicits a cellular swelling, which reduces the diffusion across the lateral plasma membranes. This effect masks the polyene effect especially for molecules showing a mainly cellular permeation pathway such as amides and lipid soluble molecules.

Acetamides↗