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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

ACTH secretion from mouse pituitary tumor cells is inhibited by loop diuretic drugs.

Stilbene disulfonate and phenylanthranilic acid derivatives block Cl- transport and ACTH secretion from mouse AtT-20 clonal corticotrophs. This study was to determine whether antagonism of Na+/K+/Cl- co-transport by loop diuretics (furosemide or bumetanide) and thereby Cl- entry could block ACTH secretion. Activity of the Na+/K+/Cl- co-transporter (symport) was measured as ouabain-insensitive, loop diuretic-sensitive uptake of 86Rb. Ouabain-insensitive uptake (80% of total 86Rb uptake) was linear over 10 min and was markedly reduced by furosemide. Substitution of Na+ by choline or Cl- by gluconate resulted in an 82 and 55% decrease, respectively, in 86Rb uptake. Furosemide and bumetanide incompletely inhibited 86Rb uptake (maximal inhibition of 60% and 69%, respectively; IC50: 1.6 x 10(-5) and 3 x 10(-6) M, respectively). Forskolin did not affect the activity of the Na+/K+/Cl- co-transporter but both basal and forskolin-stimulated secretion of ACTH were inhibited by furosemide (IC50 of 5 x 10(-4) M; maximal inhibition: 50%). Bumetanide did not affect forskolin-induced cAMP synthesis. Use of cyclamate or gluconate in place of Cl- also resulted in the inhibition of basal and forskolin-stimulated ACTH secretion. The data support the belief that inhibition of Cl- entry into AtT-20 cells by way of an Na+/K+/Cl- co-transporter can result in the inhibition of ACTH secretion but that other anion entry mechanisms may also be coupled to the secretory response in these cells.[1]


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