Feedback inhibition of sodium uptake in K+-depolarized toad urinary bladders

摘要: Abstract Ouabain-blocked toad urinary bladders were maintained in Na+-free mucosal solutions, and a depolarizing solution of high K+ activity containing only 5 mM Na+ on the serosal side. Exposure to sodium (20 activity) evoked transient amiloride-blockable inward current, which decayed near zero within one hour. The apical conductance increased initial phase current decay decreased second phase. decrease required Ca2+ be present side was more rapid when higher. At 20 3 (maximal) rate inhibition amounted 20% 10 min. could accelerated by raising mM. reversed lowering μM and, addition, zero. surface ionophore nystatin abolished sensitivity transcellular conductance, showing that Ca2+-sensitive resides membrane. data imply K+-depolarized epithelia, cellular Ca2+, taken up from medium means Na+-Ca2+ antiport, cause feedback blockage channels. However, is small, such this regulatory mechanism will have little effect at 1 less than Na+.