1,721,103 research outputs found
Protective effect of hydrocortisone on vasopressin response in frog skin
No full textThe effect of microtubular-poisons, such as colchicine and vincristine, on frog skin permeability has been investigated. Three-hour treatment with the drugs has no effect on nonelectrolyte basal transepithelial permeability, but completely suppresses the effect of ADH. Colchicine and vincristine, in addition, affect both basal sodium transport and the rise in short circuit current induced by vasopressin. The inhibition produced by microtubular-poisons disappears, however, when hydrocortisone, a glucocorticoid known to preserve junctional communications is used. Together with the results previously obtained with isolated epithelial cells (Svelto et al. 1979), these findings provide further support for our hypothesis that the microtubular-microfilament-system, is involved in cell-to-cell exchange
Calcium role in base-line and ADH-stimulated sodium transport in frog skin
No full textTreatment of ventral frog skin with serosal A23187 calcium ionophore caused an initially transient increase in transepithelial sodium transport. After 60 min of treatment with A23187, a steady-state transport value was reached which was significantly lower than the initial one. Furthermore, it was found that ionophore treatment greatly inhibited the natriferic response to ADH and to 8br-cAMP. A further analysis on the possible ionophore action mechanism was carried out through pretreatment of the skin with indomethacin, very powerful prostaglandin synthesis inhibitor. In the experimental conditions reported, A23187 seems no longer capable of inducing a transient increase in sodium transport, although it does inhibit the natriferic response to ADH
Evidence for the role of calcium in the hydrosmotic response to antidiuretic hormone in frog skin
No full textTreatment with the calcium ionophore A23187 on either the serosal or mucosal sides of frog skin, strongly inhibits the hydrosmotic response to vasopressin. On the contrary, the hydrosmotic response to 8-br-cAMP is not affected by treatment with the A23187. Trifluoperazine, a drug which inhibits the Ca2+-calmodulin complex, selectively inhibits vasopressin-induced water transport. Collectively, our results suggest that an increase in the intracellular concentration of Ca2+, obtained by treatment with the ionophore A23187, interferes with a pre-cAMP step of the hydrosmotic response to the antidiuretic hormone. Calcium ions could regulate adenyl-cyclase activity and consequently intracellular levels of cAMP. This effect may probably involve calmodulin
Local modulation of Cystic Fibrosis Conductance Regulator: cytoskeleton and compartmentalised cAMP signalling.
No full textThe cystic fibrosis conductance regulator (CFTR) is a cAMP-regulated Cl(-) channel expressed predominantly at the apical membrane of secreting epithelial cells. Mutations in the CFTR gene lead to cystic fibrosis, the most frequent genetic disease in the Caucasian population. The most common mutation, a deletion of phenylalanine at position 508 (F508del), impairs CFTR folding and chloride channel function. Although an intense effort is underway to identify compounds that target the F508del CFTR structural defect and promote its expression and stability at the plasma membrane, so far their clinical efficacy has proven to be poor, highlighting the necessity to better understand the molecular mechanism of CFTR regulation and of the pathogenesis of the disease. Accumulating evidence suggests that the inclusion of the CFTR in macromolecular complexes and its interaction with the cortical cytoskeleton may play a key role in fine-tuning the regulation of channel function. Here we review some recent findings that support a critical role for protein-protein interactions involving CFTR and for the cytoskeleton in promoting local control of channel activity. These findings indicate that compounds that rescue and stabilise CFTR at the apical membrane may not be sufficient to restore its function unless the appropriate intracellular milieu is also reconstituted
Facilitated transport of urea across the gall-bladder luminal membrane
No full textCounterflow 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
Separate regulatory control of apical and basolateral Na+/H+ exchange in renal epithelial cells
No full textcAMP levels and alpha and beta receptors stimulation by noradrenaline in frog skin.
No full textThe effect of noradrenaline on intracellular levels of cAMP in epithelial cells isolated from frog skin, has been studied both in the presence and in the absence of alpha (phentolamine) or beta (propranolol) adrenergic blocking agents. Such levels are increased by hormonal treatment and are linked to the stimulation of beta-adrenergic receptors, while alpha-stimulation has an inhibitory effect. Higher levels of cAMP are reached in the presence of both Ca2+ and Mg2+, confirming the existence of a Ca2+ and Mg2+-dependent adenyl-cyclase, stimulated by noradrenaline. The experimental conditions necessary to induce the highest intracellular cAMP levels, are those in which the permeabilizing effect reaches its maximu
Effect of cycloheximide on urea facilitated transport through toad gallbladder epithelium
No full textTransepithelial urea outfluxes across toad gallbladder were determined before and after the addition of cycloheximide. The drug inhibits the movement of urea but has no effect on thiourea and antipyrine outfluxes. The inhibition of amide transport is time dependent as also shown in counterflow experiments. These results are consistent with the hypothesis that cycloheximide inhibits the synthesis of membrane proteic sites involved in urea mediated transport
Permeability pathways for non-electrolytes through Bufo bufo gall-bladder
No full textAmphotericin 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
- …
