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C Lippe

Publications and source records attributed to C Lippe.

At least 19 recordsLinked to original sources

The nature of Cl- secretion, induced by carbaryl, across the isolated skin of Rana esculenta.

1. The pesticide carbaryl induces Cl- secretion through the isolated frog skin. 2. This effect is due to the activation of both processes responsible for this phenomenon: (a) Na+/K+/2Cl- cotransport on the serosal membrane; (b) Cl- selective channels on the external membrane. 3. Cl- outflux is inhibited by bumetanide (10(-5) M) on the serosal side and by diphenylamine-2-carboxylic acid (DPC) (10(-3) M) on the external side. 4. The DPC action is not mimicked by Naproxen, a specific inhibitor of cyclooxygenase. 5. A comparison with isoprenaline, demonstrates that the carbaryl action is, paradoxically, more selective than that of isoprenaline. 6. This selectivity of carbaryl action on Cl- permeability is confirmed by the fact that, unlike isoprenaline, carbaryl does not affect the permeability of Na+ and thiourea.

Animals

Beta 2-adrenergic regulation of urea permeability of the Bufo bufo bladder.

1. Isoprenaline strongly increases the urea permeability of the bladder of Bufo bufo. This effect is due to its interaction with beta 2-adrenoreceptors, activating, in turn, the adenyl cyclase. 2. In order to ensure the regulation of urea permeability, the isoprenaline effect is present even in pathophysiological conditions, inhibiting the vasopressin action.

Adenine

Actions of vasopressin and isoprenaline on the ionic transport across the isolated frog skin in the presence and the absence of adenyl cyclase inhibitors MDL12330A and SQ22536.

1. The effects of both adenyl cyclase inhibitors (MDL12330A and SQ22536) have been studied on the ionic transport induced by vasopressin and isoprenaline across the frog skin. 2. MDL12330A inhibits the vasopressin action on the short-circuit current (SCC), confirming that this effect is cAMP-mediated. 3. On the other hand, isoprenaline action on the SCC is unaffected by MDL12330A. However, this lack of effect is not a sufficient argument against the role of cAMP in this action; in fact, as MDL12330A is also an inhibitor of cAMP phosphodiesterase, this action could mask the inhibitory effect of the drug on adenyl cyclase. 4. By using the other adenyl cyclase inhibitor (SQ22536), probably deprived of effect on the cAMP phosphodiesterase, we obtained a strong inhibition of isoprenaline action on the SCC. Thus we conclude that the actions of isoprenaline on the ionic transport across the frog skin are also cAMP-mediated.

3',5'-Cyclic-AMP Phosphodiesterases

Actions of carbaryl on the ionic transport across the isolated skin of Rana esculenta.

1. Carbaryl, a carbamate used as a pesticide, increases the short-circuit current (SCC) across the isolated frog skin in a dose-dependent manner. 2. This effect is due to the stimulation of sodium absorption and chloride secretion. 3. Carbaryl action on short-circuit current is unrelated to its inhibitory power on cholinesterase; this statement is supported by two experimental results: (a) carbaryl is equally active on both sides of the skin, (b) atropine pretreatment does not inhibit the carbaryl action on SCC.

Animals

Diazepam effects on frog skin cyclic nucleotide phosphodiesterase.

1. The activities of cAMP phosphodiesterases (cAMP-PDE) have been measured in the homogenate of the skin of Rana esculenta. 2. The tissue possesses two distinct enzymes: a "low" Km PDE (Km = 0.42 x 10(-6) M; Vmax = 16 pmol/mg protein/min) and a "high" Km PDE (Km = 180 x 10(-6) M; Vmax = 2853 pmol/mg prot/min). Only the "high" Km form is stimulated by calcium. 3. Diazepam (1-0.5 mM) significantly inhibits both enzymes, the inhibition being of competitive type.

3',5'-Cyclic-AMP Phosphodiesterases

Permeability properties of the Bufo bufo bladder as affected by isoprenaline and vasopressin.

Isoprenaline, a beta adrenergic agonist, strongly increases both transepithelial fluxes across the urinary bladder of Bufo bufo; this effect is dose dependent, 10(-6)M being necessary for the maximal action. This effect is less selective than that of vasopressin: the ratio J urea/J thiourea is 3.8 under isoprenaline and 30.4 under vasopressin treatment. Both hormones differently affect the permeability of a mainly liposoluble molecule, i.e. antipyrine: vasopressin increases antipyrine permeability, while isoprenaline decreases it. Moreover diethylpyrocarbonate treatment of the luminal membrane strongly inhibits vasopressin effect on urea permeability leaving unmodified that of isoprenaline. However, the actions of both hormones are not additive. These results allows to assume that the tissue has a feedback mechanism which inhibits other hormonal action while the bladder is stimulated by a particular hormone.

Animals

Action of forskolin on non-electrolyte permeability across the urinary bladder of Bufo bufo as compared to that of various hormones.

1. Forskolin, an activator of adenyl-cyclase in a receptor-independent manner, mimics the ADH effect on the urea and thiourea permeabilities across the toad bladder. 2. However, differently from ADH, forskolin increases the erythritol permeability across the tissue and this effect is not reproduced by two substances increasing the urea permeability (8-BrcAMP and isoprenaline). Most probably this effect of forskolin does not involve the cAMP generating system.

8-Bromo Cyclic Adenosine Monophosphate

Action of forskolin on non-electrolyte permeability across the frog skin as compared to that of vasopressin and isoprenaline.

Forskolin, a natural diterpene activating the adenyl cyclase in a receptor-independent manner, increases symmetrically both transepithelial fluxes of urea and erithrytol through the frog skin. The effect is dose-dependent, being 5 X 10(-6) M the dose necessary to obtain the maximal action. Forskolin-induced permeabilization is inversely proportional to the molecular weight of water soluble molecules (urea greater than erythritol greater than mannitol); also the permeability of a mainly lipid soluble molecule, i.e. antipyrine, is slightly increased by the diterpene. The permeability pattern is more similar to that induced by isoprenaline as compared to that elicited by vasopressin. Differently from what occurs in other tissues, small doses of forskolin (10(-8) M) are unable to potentiate the actions of vasopressin and isoprenaline on urea permeability across the frog skin. Moreover, the maximal action of forskolin is not additive with the maximal ones of isoprenaline and vasopressin.

Animals

Effect of reagents of protein functional groups on the ADH-induced urea facilitated transport across toad urinary bladder.

1--The mechanism of the vasopressin-induced, facilitated transport across toad urinary bladder was studied by treating the luminal membrane of the epithelium with the following reagents of protein functional groups: NEM (SH groups), SITS (amino groups), EEDQ (carboxylic groups), DEPC (histidine). 2--Treatment of the luminal side of the epithelium by NEM strongly inhibits the ADH-induced urea transport, leaving unmodified the effect of the hormone on the flux of antipyrine, a lipid soluble molecule. These results confirm the hypothesis that the urea carrier is of proteic nature. 3--Treatment of the luminal side by SITS strongly inhibits ADH action on urea and antipyrine permeability; thus this effect can be considered rather unspecific. 4--On the contrary the EEDQ effect is more specific; in fact treatment of the luminal side by EEDQ strongly inhibits ADH effect on the permeability of urea, slightly increasing the ADH effect on that of antipyrine. 5--Finally, the luminal treatment by diethylpyrocarbonate inhibits almost completely the ADH action on the urea fluxes, slightly increasing the hormone effect on the antipyrine ones. 6--Based on these results we conclude that carboxylic groups and the imidazolic ring are more important than the amino groups in determining the urea transport across toad bladder, in the presence of ADH.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo

Effect of vasopressin on the permeability of non electrolytes across the skins of Rana esculenta and Bufo bufo.

Maximal doses of vasopressin increase the permeability of the skins of Bufo bufo and Rana esculenta to urea, ethylene glycol, glycerol, erythritol, beta-alanine, leaving virtually unmodified that of mannitol and antipyrine. These results demonstrate that the response to vasopressin is quite different in amphibian skins as compared to the bladders. A careful analysis of the effects of vasopressin on non-electrolyte permeability as a function of their molecular weight demonstrates that hormone elicits the formation of pores with a diameter inferior to 4 A. Under vasopressin treatment the skins exhibit a selectivity for polyhydroxylated molecules as compared to urea and beta-alanine. This selectivity is not due to active of facilitated transport and is not impaired by phloretin or DTNB which selectively blocks the permeability of urea or ethylene glycol in erythrocytes. It is proposed that the site of such selectivity is located in other plasma membranes of the epithelium.

Animals

[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