AJP - Endocrinology and Metabolism, Vol 250, Issue 2 164-E168, Copyright © 1986 by American Physiological Society
Effect of valinomycin on thyroid iodide transport and TSH-stimulated cAMP formation
J. R. Sherwin and J. W. Seaford
The K+ ionophore valinomycin, in concentrations as low as 0.1 microM,
induces an inhibition of thyroid-stimulating hormone (TSH)-stimulated cAMP
formation in cat and pig thyroid slices and isolated,
trypsin-collagenase-dispersed beef thyroid cells. Valinomycin was also
shown to inhibit histamine and prostaglandin E1 stimulation of thyroid cAMP
formation. The inhibitory effect of valinomycin could be partially overcome
by elevated (81 mM) K+ concentrations. In the absence of valinomycin, the
ability of TSH to stimulate thyroid cAMP formation was dependent on
extracellular K+. Chronic removal or addition of K+ to medium bathing
thyroid sections was accompanied by inhibition of TSH-stimulated cAMP
formation. Maximum TSH stimulation was observed at an extracellular K+ of
2.7 mM. Valinomycin had no significant effect on thyroid ATP content but
did reduce the ATP-to-ADP ratio. However, chronic removal of K+ had no
effect on either ATP or the ATP-to-ADP ratio. Varying extracellular Na+
from 26 to 144 mM or addition of tetrodotoxin did not affect TSH action.
Valinomycin addition to thyroid slices was associated with a reduction in
iodide transport as measured by the ratio of tissue to extracellular iodide
concentrations. The effect of valinomycin on iodide transport was
accompanied by an increase in iodide efflux that was not greater than that
observed with perchlorate ion, suggesting a reduced recirculation of
released iodide in valinomycin-treated tissue. These findings suggest that
alterations in thyroid cell K+ permeability or intracellular K+
concentration may be accompanied by changes in TSH-induced stimulation of
thyroid cAMP formation.
