From toad bladder to kidney.
Studies using the urinary bladder of the toad to elucidate the mechanism of transepithelial ion transport are reviewed. Sodium ions are reabsorbed from bladder urine across the granular cells, accounting for all the electrical activity of this epithelium. Sodium ions enter the granular cells passively through selective sodium channels down an electrochemical gradient, mix in the intracellular "active transport pool," and are pumped actively out of the cell across the basolateral plasma membrane. The concentration of sodium within the active transport pool is normally low, 10-14 mM, with Ringer solution bathing both surfaces. The apical plasma membrane is the major resistance barrier; both vasopressin and aldosterone stimulate sodium transport across the tissue by increasing the permeability of this barrier. The apical plasma membrane is impermeable to chloride ions and they are reabsorbed passively, in response to the transepithelial electrical potential established by active sodium transport, through paracellular channels. The bladder reabsorbs 18 sodium ions per molecule of suprabasal oxygen consumed. The relatively high apical membrane resistance buffers the basolateral active transport system from changes in osmotic work in pumping sodium out of the cell over the physiologic range of transepithelial potentials.
D000450:Aldosterone / Q000494:pharmacology; D000818:Animals; D001001:Anura / Q000378:metabolism; D001693:Biological Transport, Active / Q000187:drug effects; D002712:Chlorides / Q000378:metabolism; D007668:Kidney / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects; D012964:Sodium / Q000378:metabolism; D001743:Urinary Bladder / Q000378:metabolism* / Q000502:physiology; D014667:Vasopressins / Q000494:pharmacology; D014867:Water / Q000378:metabolism
D002712:Chlorides; D014867:Water; D014667:Vasopressins; D000450:Aldosterone; D012964:Sodium