Homocellular regulatory mechanisms in sodium-transporting epithelia: avoidance of extinction by "flush-through".
In recent years electrophysiologic studies on several sodium-transporting epithelia have uncovered two "homocellular" (intrinsic) regulatory mechanisms that appear to protect the absorptive cells from marked changes in sodium and potassium content in response to rapid and wide-ranging physiologic variations in the rate of transcellular sodium transport. These are: 1) an inverse relation between intracellular sodium activity and the sodium conductance of the apical (mucosal) membrane, and 2) a parallel relation between the rate of sodium extrusion from the cell across the basolateral membrane ("pump activity") and the conductance of that barrier to potassium. The purpose of this review is to document these homocellular regulatory mechanisms, discuss their physiologic significance, and speculate on possible underlying mechanism(s).
D000584:Amiloride / Q000494:pharmacology; D000666:Amphotericin B / Q000494:pharmacology; D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002118:Calcium / Q000502:physiology; D002462:Cell Membrane / Q000502:physiology; D003106:Colon / Q000502:physiology; D004553:Electric Conductivity; D004848:Epithelium / Q000502:physiology*; D007365:Intercellular Junctions / Q000502:physiology; D007413:Intestinal Mucosa / Q000502:physiology; D008564:Membrane Potentials; D009337:Necturus; D011817:Rabbits; D012964:Sodium / Q000502:physiology*; D001743:Urinary Bladder / Q000502:physiology
D000584:Amiloride; D000666:Amphotericin B; D012964:Sodium; D002118:Calcium