Relation between pH regulation and iodide transport in turtle thyroid glands.
Mechanisms of pH recovery after alkalinization and acidification by exposing or prepulsing turtle thyroid slices with a Hanks' balanced salt solution (HBSS) containing NH4Cl or CO2 were studied by examining the effects of amiloride, 4-acetamido-4'-isocyanostilbene-2,2'-disulphonic acid (SITS), frusemide and acetazolamide, and of reducing the concentration of Na+ or Cl- in the incubation medium. When alkalinization was produced either during exposure to NH4Cl or after a CO2 pulse, the pH in thyroid slices rose rapidly and then recovered gradually. Addition of SITS (0.1 mmol/l) or reduction of the Cl- concentration markedly inhibited pH recovery. However, amiloride (0.1 mmol/l) and low Na+ in the medium had no significant effect on recovery from alkalinization induced by NH4Cl exposure or by a CO2 pulse. These data suggest that pH recovery from alkalinization in turtle thyroid gland is achieved by an exchange of internal HCO3- for external Cl-. When acidification was accomplished by either exposure to CO2 or removal of NH4Cl, the pH of thyroid slices fell rapidly and then recovered gradually. If amiloride was added or the Na+ concentration in the medium was reduced, the pH recovery was greatly attenuated. However, SITS and low Cl- in the medium did not affect the recovery from an acid load in turtle thyroid slices. These results suggest that pH recovery from acidification in turtle thyroid gland is achieved by an exchange of internal H+ for external Na+. Both frusemide and acetazolamide prevented the pH recovery in turtle thyroid slices during exposure to and withdrawal from NH4Cl. These results suggest that besides the Na(+)-H+ and Cl(-)-HCO3- exchange processes, other mechanisms may also be involved in pH regulation in turtle thyroid glands. Simultaneous uptakes into turtle thyroid slices of 125I- and 22Na+ and of 125I- and 36Cl- were studied during and following exposure to NH4Cl in the absence and presence of different transport inhibitors, such as frusemide, amiloride, SITS and acetazolamide. When the thyroid slices were exposed to HBSS containing 30 mmol/l NH4Cl (alkalinization phase), the tissue/medium (T/M) ratios of 125I- increased gradually, reached the highest point in 10 min, and were maintained at this level for the next 20 min. The T/M ratios of 22Na+ and 36Cl- of thyroid slices also slowly increased after exposure to NH4Cl.(ABSTRACT TRUNCATED AT 400 WORDS)
Chow
S Y
SY
Department of Physiology, University of Utah School of Medicine, Salt Lake City 84108.
Woodbury
D M
DM
Yen-Chow
Y C
YC
D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid; D000086:Acetazolamide; D000584:Amiloride; D000643:Ammonium Chloride; D000818:Animals; D001692:Biological Transport; D002245:Carbon Dioxide; D002712:Chlorides / Q000378:metabolism; D004114:Dimethadione; D005110:Extracellular Space / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D007444:Inulin / Q000378:metabolism; D007454:Iodides / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism; D013961:Thyroid Gland / Q000378:metabolism*; D014426:Turtles / Q000378:metabolism*; D014867:Water / Q000378:metabolism
D002712:Chlorides; D007454:Iodides; D000643:Ammonium Chloride; D014867:Water; D002245:Carbon Dioxide; D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid; D000584:Amiloride; D007444:Inulin; D012964:Sodium; D004114:Dimethadione; D000086:Acetazolamide