Document Detail

Ouabainlike compound in hypertension associated with ectopic corticotropin syndrome.
MedLine Citation:
PMID:  8794827     Owner:  NLM     Status:  MEDLINE    
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.
A Goto; K Yamada; H Hazama; Y Uehara; K Atarashi; Y Hirata; K Kimura; M Omata
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Publication Detail:
Type:  Case Reports; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Hypertension     Volume:  28     ISSN:  0194-911X     ISO Abbreviation:  Hypertension     Publication Date:  1996 Sep 
Date Detail:
Created Date:  1996-11-22     Completed Date:  1996-11-22     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  421-5     Citation Subset:  IM    
Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
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MeSH Terms
ACTH Syndrome, Ectopic / blood*,  etiology,  urine*
Chromatography, High Pressure Liquid
Hypertension / blood*,  etiology,  urine*
Lung Neoplasms / complications
Middle Aged
Ouabain / blood*,  urine*
Reg. No./Substance:

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