title: Renal ontogeny: epithelial transport in the mammalian mesonephric proximal tubule.
abstract: The role of the mammalian mesonephric kidney is not completely understood. It has been established that outpouchings of the mesonephric excretory ducts give origin to parts of the urogenital system of the adult. It is also known that mammalian mesonephric urine is formed as an ultrafiltrate. The mesonephric renal tubules have Na+/K+ adenosine triphosphatase (Na+/K+ pump), secrete phenol red, and reabsorb protein. Prior to this work, the possibility of epithelial transport of ions and metabolic substrates across mammalian mesonephric tubules had not been directly evaluated. Proximal mesonephric tubules obtained from 17 to 18-days-old rabbit embryos were isolated and perfused in vitro. Continuous intracellular electrical recordings were obtained with Ling-Gerard-type microelectrodes and a high input impedance electrometer. In tubules perfused and bathed in standard mammalian Ringer's solutions, the average transmembrane electrical cell potential difference (PD) was -43 +/- 0.5 mV (76 cells). The cellular PD decreased by 30 percent when the temperature of the bath was cooled from 37 degrees C to 30 degrees C. The cells also depolarized by 25 percent in the first five minutes of exposure to 0.1 mM ouabain. In addition, the cell PD decreased by 40 and 60 percent when the extracellular potassium concentration was raised from five to 25 and 50 mM, respectively. The uptake of glucose and alanine was similarly electrogenic (delta:1 mV/mM). The cell PD, the K+ conductance, and the electrogenicity induced by luminal exposure to 5 mM glucose or alanine are significantly lower in the mesonephric as compared to the metanephric proximal tubules of the rabbit. These observations suggest that sodium-coupled transepithelial transport mechanisms, driven by the Na+/K+ pump, are already present in the mammalian mesonephric proximal tubule. Increases in the number of Na+/K+ pumps, conductive K+ channels, and sodium-substrate cotransporters seem to be at the core of proximal tubular ontogeny.
authors.affiliation: Renal Pathology Laboratory, V.A. Medical Center, Salt Lake City, UT 84148.
authors.forename: D A
authors.initials: DA
authors.lastname: Terreros
authors.forename: K
authors.initials: K
authors.lastname: Tiedemann
mesh_terms: D000818:Animals; D001693:Biological Transport, Active; D004848:Epithelium / Q000502:physiology; D007687:Kidney Tubules, Proximal / Q000196:embryology* / Q000201:enzymology; D008650:Mesonephros / Q000196:embryology* / Q000201:enzymology; D011188:Potassium / Q000378:metabolism; D015221:Potassium Channels / Q000378:metabolism; D011817:Rabbits; D015222:Sodium Channels / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
chemical_list: D015221:Potassium Channels; D015222:Sodium Channels; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium