Influence of serosal Cl on transport properties and cation activities in frog skin.
The effects of serosal substitution of isosmotic Na2SO4-Ringer solution for NaCl-Ringer solution were studied in the short-circuited frog skin (Rana pipiens, Northern variety). Despite prompt changes of transepithelial measurements, initial cellular effects were slight. After 30 to 45 min, however, the transcellular current had decreased and the cell electrical potential had depolarized, in association with decrease of the apical membrane fractional resistance and basolateral membrane conductance. Apical membrane slope conductance was unaffected. Similar effects were obtained with isolated epithelia. With the use of gluconate or NO3 in place of Cl, the effects on cellular current and conductance were minimal or insignificant, despite changes of the cell potential, fractional resistance, and basolateral conductance similar to those seen with sulfate. Following prolonged exposure to serosal SO4-Ringer, the extent of depolarization induced by raising the serosal K concentration decreased, indicating diminution of basolateral K conductance and the existence of other basolateral conductances. Equilibration in serosal gluconate-Ringer enhanced polarization on serosal restoration of Cl or removal of Na, again indicating a time-dependent change in the basolateral conductance pattern. Depolarization on removal of serosal Cl was not attributable to inhibition of the pump. Nor was it the result of decrease of the K equilibrium potential EK: exposure to serosal SO4-Ringer decreased cell K activity aKc from 104 +/- 6 to 58 +/- 4 mM (n = 5), but EK was reduced only slightly; exposure to serosal gluconate increased aKc and EK. Serosal sulfate lowered the cell Na activity aNac, but the electrochemical potential difference for Na across the apical surface was unaffected. The concurrent decrease of both aKc and aNac following serosal substitution of SO4 for Cl raises questions concerning mechanisms of osmoregulation.
Klemperer
G
G
Department of Physiology, Boston University School of Medicine, Massachusetts 02118.
Essig
A
A
D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D001693:Biological Transport, Active; D002712:Chlorides / Q000378:metabolism / Q000502:physiology*; D004553:Electric Conductivity; D005942:Gluconates / Q000494:pharmacology; D066298:In Vitro Techniques; D008566:Membranes / Q000502:physiology; D009566:Nitrates / Q000494:pharmacology; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000502:physiology; D011894:Rana pipiens; D012867:Skin / Q000378:metabolism*; D012879:Skin Physiological Phenomena; D012964:Sodium / Q000502:physiology; D013431:Sulfates / Q000494:pharmacology
D002712:Chlorides; D005942:Gluconates; D009566:Nitrates; D013431:Sulfates; C012036:sodium sulfate; D010042:Ouabain; D000584:Amiloride; C031618:sodium nitrate; D012964:Sodium; C030691:gluconic acid; D011188:Potassium