OUABAIN-LIKE COMPOUND IN HYPERTENSION ASSOCIATED WITH ECTOPIC CORTICOTROPIN SYNDROME

Molecular mechanisms related to sodium retention have been implicated in the pathogenesis of hypertension. It is unclear how sodium retentio n leads to a rise in blood pressure, but ouabainlike compound may act as a final common pathway in sodium-induced hypertension. In ectopic c orticotropin syndrome, hypertension has been attributed to cortisol in activation overload, giving rise to mineralocorticoid-type hypertensio n. We sequentially measured plasma and urinary levels of ouabainlike c ompound over 2 months to evaluate its role in the hypertensive mechani sms in a 64-year-old man with this syndrome caused by lung cancer. His data included hypokalemia and increased cortisol concentrations, cort icotropin levels, and urinary 17-hydroxycorticosteroid excretion. Plas ma renin activity was suppressed. Plasma and urinary levels of ouabain like compound were markedly increased concomitantly with high blood pr essure. The maximum plasma level was 40-fold the normal range of the s ubject. After chemotherapy, ouabainlike compound levels gradually decr eased in parallel with the decline in blood pressure and rise in potas sium concentration. A correlation was observed between plasma and urin ary levels of ouabainlike compound (P < .05). plasma and urinary level s of ouabainlike compound correlated with systolic (P < .01) and diast olic (P < .05) pressures, respectively. The peak of ouabainlike compou nd in plasma and urine coincided with that of authentic ouabain on hig h-performance liquid chromatography. Ouabainlike compound derived from urine inhibited [H-3]ouabain binding to human erythrocytes. These fin dings suggest that ouabainlike compound with biological activity could partly account for hypertension in ectopic corticotropin syndrome.