Active Ca2+ reabsorption in the proximal tubule of the rat kidney. Dependence on sodium- and buffer transport

Pflugers Arch. 1976 Aug 24;364(3):223-8. doi: 10.1007/BF00581759.

Abstract

Using the stop flow microperfusion technique with simultaneous capillary perfusion the rate active Ca2+ reabsorption was evaluated by measuring the static head electrochemical potential difference as well as the permeability of the tubular wall for Ca2+ ions. Under control conditions the active Ca2+ transport was calculated to be 3.35 X 10(-13) mol/cm - s. It declined toward zero if the ambient Na+ was replaced by choline or lithium. Parallel experiments in the golden hamster showed that active Ca2+ transport, vanished completely if active Na+ transport was blocked by ouabain (1 mM). These data indicate that the active Ca2+ reabsorption from the proximal tubule depends on the active reabsorption of Na2+ presumably via a Na+-Ca2+ countertransport at the contraluminal cell membrane. The static head electrochemical potential difference of Ca2+ is the same in late and early proximal tubules. It is also not affected by the presence of acetazolamide (10(-4) M) by the absence of bicarbonate or glycodiazine buffer or by the absence or presence of phosphate (2 mM).

MeSH terms

  • Acetazolamide / pharmacology
  • Animals
  • Bicarbonates / metabolism
  • Biological Transport, Active
  • Buffers
  • Calcium / metabolism*
  • Cell Membrane Permeability
  • Choline / pharmacology
  • Kidney Tubules, Proximal / metabolism*
  • Lithium / pharmacology
  • Male
  • Ouabain / pharmacology
  • Rats
  • Sodium / metabolism*

Substances

  • Bicarbonates
  • Buffers
  • Ouabain
  • Lithium
  • Sodium
  • Choline
  • Acetazolamide
  • Calcium