Evidence for OH−/H+ permeation across the peritubular cell membrane of rat renal proximal tubule in HCO3−-free solutions

1987 ◽  
Vol 409 (1-2) ◽  
pp. 132-137 ◽  
Author(s):  
B. C. Burckhardt ◽  
E. Frömter
Keyword(s):  
Cell Membrane ◽  
Proximal Tubule ◽  
Renal Proximal Tubule ◽  
Rat Renal Proximal Tubule

The Fine Structure of Rat Renal Microbodies and Cytoplasmic Bodies Following Perfusion Fixation

1973 ◽  
Vol 31 ◽  
pp. 620-621
Author(s):  
J. M. Barrett ◽  
P. M. Heidger
Keyword(s):  
Fine Structure ◽  
Proximal Tubule ◽  
Rat Kidney ◽  
Renal Proximal Tubule ◽  
Convincing Evidence ◽  
Cytoplasmic Bodies ◽  
Rat Renal Proximal Tubule ◽  
Renal Proximal Tubule Cells ◽  
Perfusion Fixation

Microbodies have received extensive morphological and cytochemical investigation since they were first described by Rhodin in 1954. To our knowledge, however, all investigations of microbodies and cytoplasmic bodies of rat renal proximal tubule cells have employed immersion fixation. Tisher, et al. have shown convincing evidence of fine structural alteration of microbodies in rhesus monkey kidney following immersion fixation; these alterations were not encountered when in vivo intravascular perfusion was employed. In view of these studies, and the fact that techniques for perfusion fixation have been established specifically for the rat kidney by Maunsbach, it seemed desirable to employ perfusion fixation to study the fine structure and distribution of microbodies and cytoplasmic bodies within the rat renal proximal tubule.

Hormonal regulation of rat renal proximal tubule brush-border membrane ionic permeability

1992 ◽  
Vol 263 (1) ◽  
pp. F144-F151 ◽  
Author(s):  
M. S. Lipkowitz ◽  
R. D. London ◽  
J. C. Beck ◽  
R. G. Abramson
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Brush Border ◽  
Renal Proximal Tubule ◽  
Ionic Permeability ◽  
Brush Border Membranes ◽  
Rat Renal Proximal Tubule ◽  
Selective Increase ◽  
Gi Proteins ◽  
Cl Permeability

The effects on ionic permeability of toxins and hormones that activate or deactivate the guanine nucleotide regulatory (G) proteins that govern adenylate cyclase activity were examined in rat renal proximal tubule cell brush-border membranes. These studies demonstrate that activation of stimulatory G (Gs) proteins by cholera toxin or parathyroid hormone and deactivation of inhibitory (G (Gi) proteins by pertussis toxin result in a selective increase in Cl- permeability relative to that of K+ as determined with the potential-sensitive fluorescent probe 3,3'-dipropylthiadicarbocyanine iodide [diS-C3-(5)]. In contrast, activation of Gi by angiotensin II significantly decreases relative Cl- permeability. The selective increase in relative Cl- permeability induced by parathyroid hormone results in an inside-negative potential in membrane vesicles exposed to an inward NaCl gradient that is of sufficient magnitude to stimulate electrogenic, Na(+)-dependent glucose transport. These data suggest that the relative ionic permeabilities of brush-border membranes are tonically regulated by the opposing effects of hormones that act via Gs or Gi proteins. Changes in membrane potential resulting from this regulation may play an important role in modifying transport in the proximal tubule.

Effect of hypermagnesemia on rat jejunal sodium and water transport

1976 ◽  
Vol 231 (6) ◽  
pp. 1771-1776 ◽  
Author(s):  
GF DiBona ◽  
LL Sawin
Keyword(s):  
Proximal Tubule ◽  
Water Transport ◽  
Renal Proximal Tubule ◽  
Epithelial Tissue ◽  
Rat Jejunum ◽  
Water Reabsorption ◽  
Sodium Influx ◽  
Sodium Efflux ◽  
Rat Renal Proximal Tubule

Hypermagnesemia decreases sodium and water reabsorption in the rat renal proximal tubule. To further understand this action, the effect of hypermagnesemia on sodium and water transport in the in vivo perfused rat jejunum was studied. The rat jejunum was chosen as another transporting epithelial tissue in the same species with unidirectional sodium flux characteristics similar to the rat renal proximal tubule, i.e., leaky as opposed to tight. Hypermagnesemia decreased net jejunal sodium and water reabsorption. This decrease was due to a reduction in unidirectional sodium efflux from lumen to blood and not to an increase in unidirectional sodium influx from blood to lumen. Hypermagnesemia did not change the jejunal permeability to inulin. The effect of hypermagnesemia on jejunal sodium and water transport is similar to that renal proximal tubule sodium and water transport. This similarity suggests that the mechanism of action of magnesium of these two transporting epithelial tissues is similar.

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