Ohashi M, Higuchi K, Hashiguchi T, Takayanagi R, Nawata H
Third Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka.
Fukuoka Igaku Zasshi. 1991 Mar;82(3):101-4.
The previous study demonstrated that the aldosterone secretion of aldosterone-producing adrenocortical adenoma failed to be suppressed by human atrial natriuretic peptide, based on the data in synthetic alpha-human atrial natriuretic peptide infusion in vivo and the effect on in vitro secretion from cultured adenoma cells. Using the membrane fractions prepared from human adrenal tissues and an aldosterone-producing adenoma tissues, we characterized the binding sites for [125I] alpha-human atrial natriuretic peptide by the binding study and affinity-labeling of [125I] alpha-human atrial natriuretic peptide. Both normal adrenal and adenoma tissue membrane fractions possessed specific binding sites, however the relative binding capacity for [125I] alpha-human atrial natriuretic peptide in the adenoma preparations was markedly lower than that in the normal adrenal tissue preparation. The specific binding sites for [125I] alpha-human atrial natriuretic peptide were detected at the region of 140 KD and 67-70 KD only in the normal adrenal membrane fractions. Our data suggest that the refractoriness to the effect of atrial peptide may be due to the reduced receptor sites in aldosterone-producing adenoma cells.