Use of transgenic animals to study renal acid-base transport.
Many of the transporters mediating renal acid-base homeostasis have recently been identified at the molecular level. These advances have made it possible to generate transgenic mice with deficiency or overexpression of specific transporter isoforms. Such knockout mice have served as useful experimental models to quantitate the contribution of a given transporter isoform to transtubular acid-base transport along the nephron. Studies with transgenic and knockout mice have also been used to elucidate the compensatory adaptive mechanisms in response to specific transport deficiencies. We review experiments using transgenic mice to evaluate the physiological roles in acid-base transport of NHE isoforms, vacuolar H+ pump subunits, H+, K(+)-ATPase isoforms, carbonic anhydrase, Cl(-)-base exchangers and such regulatory mediators as nitric oxide and endothelin.
Wang
Tong
T
Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06520-8026, USA. Tong.Wang@yale.edu
Giebisch
Gerhard
G
Aronson
Peter S
PS
D000136:Acid-Base Equilibrium / Q000502:physiology*; D000818:Animals; D030801:Animals, Genetically Modified; D001692:Biological Transport; D002256:Carbonic Anhydrases / Q000378:metabolism; D027963:Chloride-Bicarbonate Antiporters / Q000378:metabolism; D007668:Kidney / Q000378:metabolism*; D020033:Protein Isoforms / Q000378:metabolism; D006180:Proton-Translocating ATPases / Q000378:metabolism; D017923:Sodium-Hydrogen Exchangers / Q000378:metabolism
D027963:Chloride-Bicarbonate Antiporters; D020033:Protein Isoforms; D017923:Sodium-Hydrogen Exchangers; D006180:Proton-Translocating ATPases; D002256:Carbonic Anhydrases