Effect of parathyroid hormone on acid/base transport in rabbit renal proximal tubule S3 segment

1993 ◽  
Vol 423-423 (1-2) ◽  
pp. 7-13 ◽  
Author(s):  
George Seki ◽  
Shigeo Taniguchi ◽  
Shu Uwatoko ◽  
Keiji Suzuki ◽  
Kiyoshi Kurokawa
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Renal Proximal Tubule ◽  
Acid Base ◽  
S3 Segment

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.

scholarly journals Defective Parathyroid Hormone Regulation of NHE3 Activity and Phosphate Adaptation in Cultured NHERF-1-/-Renal Proximal Tubule Cells

2004 ◽  
Vol 279 (36) ◽  
pp. 37815-37821 ◽  
Author(s):  
Rochelle Cunningham ◽  
Deborah Steplock ◽  
Fengying Wang ◽  
Huijun Huang ◽  
Xiaofei E ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Renal Proximal Tubule ◽  
Hormone Regulation ◽  
Proximal Tubule Cells ◽  
Tubule Cells ◽  
Renal Proximal Tubule Cells

Na-HCO3 cotransport and Na-H antiporter in chronic respiratory acidosis and alkalosis

1989 ◽  
Vol 256 (3) ◽  
pp. F414-F420 ◽  
Author(s):  
O. S. Ruiz ◽  
J. A. Arruda ◽  
Z. Talor
Keyword(s):  
Proximal Tubule ◽  
Respiratory Acidosis ◽  
Renal Proximal Tubule ◽  
Transport Systems ◽  
Acid Base ◽  
Basolateral Membranes ◽  
Two Systems ◽  
22Na Uptake ◽  
And Control

Renal acidification in renal proximal tubule is thought to be mediated by luminal Na-H antiporter and the HCO3- generated by this antiporter is removed from the cell by a basolateral Na-HCO3 cotransporter. To study the effect of respiratory acid-base disorders on these transport systems, we have measured the Na-HCO3 cotransport in basolateral membranes and Na-H antiporter in luminal membranes in control rabbits, rabbits exposed to 10% CO2 (chronic hypercapnia), and rabbits exposed to 10% O2-90% N2 (chronic hypocapnia). The Vmax of HCO3(-)-dependent 22Na uptake was significantly higher in chronic hypercapnia than controls (2.54 +/- 0.03 vs. 1.18 +/- 0.21 nmol.mg protein-1.3 s-1, P less than 0.001). Likewise, the Vmax of the Na-H antiporter was also increased compared with controls (924.9 +/- 42.1 vs. 549.1 +/- 62.8 fluorescence units (FU).300 micrograms protein-1.min-1). In chronic hypocapnia, the Vmax of Na-HCO3 cotransport was lower than controls (0.72 +/- 0.11 vs. 1.18 +/- 0.21 nmol.mg protein-1.3 s-1, P less than 0.05). There was no difference, however, in the Vmax of the Na-H antiporter between hypocapnia and control (524.2 +/- 24.3 vs. 549.1 +/- 62.8, FU.300 micrograms protein-1.min-1). The Vmaxs of the Na-HCO3 cotransport and of the Na-H antiporter in hypocapnic, control, and hypercapnic rabbits were linearly related (r = 0.81), suggesting a simultaneous adaptation of the two systems in respiratory acid-base disorders.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Evidence for conductive Cl- pathway in the basolateral membrane of rabbit renal proximal tubule S3 segment.

1993 ◽  
Vol 92 (3) ◽  
pp. 1229-1235 ◽  
Author(s):  
G Seki ◽  
S Taniguchi ◽  
S Uwatoko ◽  
K Suzuki ◽  
K Kurokawa
Keyword(s):  
Proximal Tubule ◽  
Basolateral Membrane ◽  
Renal Proximal Tubule ◽  
S3 Segment

Mechanism of anion permeation in the basolateral membrane of isolated rabbit renal proximal tubule S3 segment

1997 ◽  
Vol 272 (3) ◽  
pp. C837-C846 ◽  
Author(s):  
G. Seki ◽  
H. Yamada ◽  
S. Taniguchi ◽  
S. Uwatoko ◽  
K. Suzuki ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Channel Blocker ◽  
Basolateral Membrane ◽  
Renal Proximal Tubule ◽  
K Channel ◽  
Anion Selectivity ◽  
Anion Permeation ◽  
S3 Segment ◽  
Cl Conductance ◽  
Higher Sensitivity

Conventional and double-barreled microelectrodes were used to examine the anion selectivity of Cl- conductance in the basolateral membrane of rabbit renal proximal tubule S3 segment. The permeability sequence determined by anion replacements in the presence of K+ channel blocker quinine was SCN- > I- > Br- > Cl- > gluconate in both nonperfused and luminally perfused tubules. The anion-selective microelectrodes with higher sensitivity to I- enabled us to measure intracellular I- activities. With these electrodes, we could compare the conductive movements of Cl- and I- in response to the increase in bath K+ concentrations and confirmed that the conductance sequence was also I- > Cl-. Although the basolateral potential changes generated by Cl- and Br- currents were stimulated by adenosine 3',5'-cyclic monophosphate (cAMP), the potential changes by SCN- and I- currents were somewhat inhibited by cAMP. In addition, the conductive uptake of I- was, in contrast to that of Cl-, inhibited by cAMP These results are consistent with the existence of at least two distinct anion conductances in this membrane, which are differently regulated by cAMP.

scholarly journals Effects of dietary Pi on the renal Na+-dependent Pi transporter NaPi-2 in thyroparathyroidectomized rats

1998 ◽  
Vol 333 (1) ◽  
pp. 175-181 ◽  
Author(s):  
Fumie TAKAHASHI ◽  
Kyoko MORITA ◽  
Kanako KATAI ◽  
Hiroko SEGAWA ◽  
Ai FUJIOKA ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Immunohistochemical Analysis ◽  
Renal Proximal Tubule ◽  
Kidney Cortex ◽  
Transport Activity ◽  
Independent Manner ◽  
Pi Transport

Dietary Pi and parathyroid hormone (PTH) are two most important physiological and pathophysiological regulators of Pi re-absorption in the renal proximal tubule. Effects of dietary Pi on Na+/Pi co-transporter NaPi-2 were investigated in thyroparathyroidectomized (TPTX) rats. NaPi-2 protein and mRNA in the kidney cortex of TPTX rats were increased ≈ 3.8- and 2.4-fold in amount respectively compared with those in the sham-operated animals. Administration of PTH to the TPTX rats resulted in a decrease in the amount of NaPi-2 protein, but not in the abundance of NaPi-2 mRNA. Deprivation of dietary Pi in the TPTX rats did not affect the amount of NaPi-2 mRNA and protein. In the Pi-deprived TPTX rats, feeding of a high-Pi diet resulted in marked decreases in Pi transport activity and the amount of NaPi-2 protein in the superficial nephrons. Immunohistochemical analysis demonstrated that administration of PTH to TPTX rats resulted in a decrease in NaPi-2 immunoreactivity from both superficial and juxtamedullary nephrons within 4 h. Switching TPTX animals from a low-Pi diet to the high-Pi diet decreased NaPi-2 immunoreactivity from superficial nephrons, but not from juxtamedullary nephrons, within 4 h. These results suggest that dietary Pi could regulate the amount of NaPi-2 protein in the superficial nephrons in a PTH-independent manner.

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