title: Ouabainlike compound in hypertension associated with ectopic corticotropin syndrome.
abstract: Molecular mechanisms related to sodium retention have been implicated in the pathogenesis of hypertension. It is unclear how sodium retention leads to a rise in blood pressure, but ouabainlike compound may act as a final common pathway in sodium-induced hypertension. In ectopic corticotropin syndrome, hypertension has been attributed to cortisol inactivation overload, giving rise to mineralocorticoid-type hypertension. We sequentially measured plasma and urinary levels of ouabainlike compound over 2 months to evaluate its role in the hypertensive mechanisms in a 64-year-old man with this syndrome caused by lung cancer. His data included hypokalemia and increased cortisol concentrations, corticotropin levels, and urinary 17-hydroxycorticosteroid excretion. Plasma renin activity was suppressed. Plasma and urinary levels of ouabainlike compound were markedly increased concomitantly with high blood pressure. The maximum plasma level was 40-fold the normal range of the subject. After chemotherapy, ouabainlike compound levels gradually decreased in parallel with the decline in blood pressure and rise in potassium concentration. A correlation was observed between plasma and urinary levels of ouabainlike compound (P < .05). Plasma and urinary levels of ouabainlike compound correlated with systolic (P < .01) and diastolic (P < .05) pressures, respectively. The peak of ouabainlike compound in plasma and urine coincided with that of authentic ouabain on high-performance liquid chromatography. Ouabainlike compound derived from urine inhibited [3H]ouabain binding to human erythrocytes. These findings suggest that ouabainlike compound with biological activity could partly account for hypertension in ectopic corticotropin syndrome.
authors.affiliation: Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Goto
authors.forename: K
authors.initials: K
authors.lastname: Yamada
authors.forename: H
authors.initials: H
authors.lastname: Hazama
authors.forename: Y
authors.initials: Y
authors.lastname: Uehara
authors.forename: K
authors.initials: K
authors.lastname: Atarashi
authors.forename: Y
authors.initials: Y
authors.lastname: Hirata
authors.forename: K
authors.initials: K
authors.lastname: Kimura
authors.forename: M
authors.initials: M
authors.lastname: Omata
mesh_terms: D000182:ACTH Syndrome, Ectopic / Q000097:blood* / Q000209:etiology / Q000652:urine*; D002851:Chromatography, High Pressure Liquid; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000209:etiology / Q000652:urine*; D008175:Lung Neoplasms / Q000150:complications; D008297:Male; D008875:Middle Aged; D010042:Ouabain / Q000097:blood* / Q000652:urine*
chemical_list: D010042:Ouabain