1,721,237 research outputs found
Brush border and basal lateral membranes in the action of thyroid hormone on the proximal tubule
No full textDeterminazione in situ ed in vivo del pH intracellulare di singole cellule tubulari mediante microscopia laser confocale
No full textThe use of micropuncture, isolated tubule, and vesicle technique in the study of the action of thyroid hormones on the proximal tubule function
No full textIn hypothyroid rats (TX), the isotonic fluid reabsorption (Jv), that is closely linked to the transepithelial sodium transport (JNa), is unpaired. The administration of physiological doses (10 μg/kg body weight per day) of tri-iodothyronine (T3) doubles Jv in three days (TX+T3J. This phenomenon could be explained by several mechanisms: (i) a direct stimulation of Na-K-A TPase, (ii) an increase in the Na+ entry step, (iii) changes in the permeability properties of the luminal and/or basal lateral membranes. Using a kinetic microassay, Na-K-ATPase activity was measured in early (S1) and late (S2) proximal tubules segments isolated from control, TX, and TX+3T3 animals. In TX rats the enzyme activity was lower (70%) in both segments versus control rats, it remained unchanged after 3 days, and it increased after 7 days of T3 substitution. The Na+ permeability of brush border membrane (BBM) vesicles isolated from TX and TX+T3 rats was identical. However the valuation of the K+ membrane permeability by in vivo perfusion of the lumen and peritubular space of proximal tubules of TX rats, with perfusate containing the K+ ionophore valinomycin (1 μg/ml), induced a significant increase in Jv that accounted for 40% of that elicited by T3. Taken together, the in vivo and in vitro experiments suggest that the early effect on Jv of physiological doses of T3 cannot be explained by a direct action of T3 either on the Na+ entry step across the BBM or on the Na+ exit step (i.e., the Na-K-ATPase), but rather by an increase in K+ permeability of proximal tubular cell membranes. This latter effect would explain the increase in Jv through an increase in the driving force for sodium. © 1985 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted
Amphotericin B and Amphotericin B methylester: Effect on brush border membrane permeability
No full textIn order to explain the nephrotoxicity of polyene antibiotics such as Amphotericin B (AM), an effect on the tubule membrane permeability has been postulated. However, studies on the action of AM have been complicated by the use of sodium deoxycholate (DOC), a membrane dissociating detergent as a solvent. Recently, a derivative, the methylester aspartate salt of Amphotericin B (AME) has been synthesized, which is highly water soluble in the absence of organic solvents. We have tested the action of AM, DOC, and AME on the sodium permeability of brush border (BBM) vesicles isolated from rat kidney cortex. It was found that both AM and AME increased the 22Na uptake as measured by a rapid filtration technique. However, a large fraction of the AM action was due to the effect of DOC on the BBM sodium permeability. We also investigated the time- and dose-dependent action of AME on 22Na and 3H-D-mannitol efflux from BBM vesicles. After 15 sec of exposure, efflux from 22Na-preloaded vesicles was unchanged in the presence of 1 μg AME/mg protein compared to control vesicles. With 10, 50, and 100 μg AME/mg protein, the efflux increased 16, 25, and 35% respectively; 260 μg AME/mg protein did not elicit a further increment in the 22Na efflux. In the same membrane vesicles 3H-D-mannitol efflux did not change. After preincubation of the membranes for 60 min with different concentrations of AME, the 15 sec 22Na efflux increased 26% in the presence of 1 μg/mg protein AME with no change in the 3H-D-mannitol efflux. At higher concentrations of AME (200 and 300 μg/mg protein), an increase in 22Na efflux (36%), but also an increased 3H-D-mannitol efflux (26 and 63% respectively) was observed. These studies demonstrate that AME increases the Na permeability of BBM in a time- and dose-dependent manner. At higher concentrations and with longer incubation periods, AME additionally affects the overall membrane permeability. The increase in sodium permeability and the breakdown in membrane barrier may be among the factors responsible for the nephrotoxocity of Amphotericin B and its derivatives
ORMONI TIROIDEI E TRASPORTO TUBULARE PROSSIMALE DI SODIO I: VARIAZIONI DELL'ATTIVITÀ DELLA NA+-K+-ATPASI DETERMINATA SU SINGOLI NEFRONI
No full textRenal bicarbonate reabsorption in the rat: I. Effects of hypokalemia and carbonic anhydrase
No full textFree-flow micropuncture studies were carried out on superficial rat proximal and distal tubules to assess the participation of different nephron segments in bicarbonate transport. Particular emphasis was placed on the role of the distal tubule, and microcalorimetric methods used to quantitate bicarbonate reabsorption. Experiments were carried out in control conditions, during dietary potassium withdrawal, and after acute intravenous infusions of carbonic anhydrase. We observed highly significant net bicarbonate reabsorption in normal acid-base conditions as evidenced by the maintenance of significant bicarbonate concentration gradients in the presence of vigorous fluid absorption. Distal bicarbonate reabsorption persisted in hypokalemic alkalosis and even steeper transepithelial concentration gradients of bicarbonate were maintained. Enhancement of net bicarbonate reabsorption followed the acute intravenous administration of carbonic anhydrase but was limited to the nephron segments between the late proximal and early distal tubule. The latter observation is consistent with a disequilibrium pH along the proximal straight tubule (S3 segment), the thick ascending limb of Henle, and/or the early distal tubule
ORMONI TIROIDEI E TRASPORTO TUBULARE PROSSIMALE DI SODIO IV: L'AZIONE DELLA TRI-IODIOTIRONINA SULLA PERMEABILITÀ AL POTASSIO DELLA MEMBRANA CELLULARE
No full text
ORMONI TIROIDEI E TRASPORTO TUBULARE PROSSIMALE DI SODIO II: LA PERMEABILITÀ AL SODIO DELLA MEMBRANA CELLULARE STUDIATA IN VIVO
No full textShort term effect of low doses of tri-iodothyronine on proximal tubular membrane Na−K-ATPase and potassium permeability in thyroidectomized rats
No full textTri-iodothyronine (T3), even when administered for short time and at low doses, induces a large increase in the isotonic fluid reabsorption (Jv) in proximal tubules of thyroidectomized rats (TX). In order to investigate the role of the Na−K-ATPase in this process, we measured the Na−K-ATPase activity in early proximal convoluted tubules (S1) and proximal straight tubules (S2) microdissected from TX rats and rats treated with low doses of T3 (10 μg/kg body wt), either for 3 days (TX+3T3) or for 7 days (TX+7T3). In both segments no changes in Na−K-ATPase activity were found in TX+3T3 rats versus TX rats, while an increase was registered in TX+7T3 rats. Using micropuncture techniques, Jv measured on the same tubular segments increased by 68% in TX+3T3 rats versus TX. Thus, no correlation between Jv and Na−K-ATPase activity measured in vitro could be detected after short term treatment of TX rats with T3. Na−K-ATPase activity in vivo is also regulated by the potassium permeability of the membrane, which might be altered by tri-iodothyronine. This hypothesis was tested by perfusing intraluminally and peritubularly proximal tubules of TX rats with the K ionophore, valinomycin (1 μg/ml). In the dual perfusion experiments valinomycin elicited 40% of the action induced on Jv by 3 days treatment with T3. On the other hand, no further increase in Jv was recorded when valinomycin was applied in TX rats pretreated with T3. Taken together, the in vivo and in vitro experiments suggest that low doses of T3 administered for short time to TX rats do not affect Na−K-ATPase activity directly, but stimulate the in vivo activity indirectly by an increase in the k permeability of proximal tubular cell membranes. This latter effect would explain the increase in Jv through an increase in the driving force for sodium entry into the cell. © 1985, Springer-Verlag. All rights reserved
- …
