Hypoadrenalism

Abstract

Considerable evidence has accumulated that both the sodium ion and the adrenal cortex are concerned to some extent with the maintenance of blood pressure levels in hypertensive patients ( 1 , 2 , 3 ). Although the rigid restriction of salt masks the pressor response of hypertensives to desoxycorticosterone( 4 ), this type of observation does not establish the fact that alterations in sodium metabolism modify the arterial tension through an adrenal mechanism. It has been noted that the adrenals of rats on a reduced sodium intake may be smaller and different in color( 5 ), temporarily depleted of ascorbic acid( 6 ), and may show secretory changes( 7 ) and (in nephritic animals) subcapsular hyperplasia ( 8 ). Furthermore, excessive salt, or liberal amounts in animals receiving desoxycorticosterone, has resulted in progressive structural and functional atrophy of the glomerular zone of the adrenal cortex( 9 , 10 ). Finally, chromatographic patterns of urinary steroid excretion may be influenced by the salt intake( 11 ).

In order to investigate further the possibility that sodium influences the blood pressure through steroidal action, studies were undertaken in a patient with uncomplicated hypertensive vascular disease and Addison's disease who also had mild diabetes mellitus and rheumatoid arthritis.

Case report and methods. G.S., a 55-year-old, white housewife, was admitted to the metabolism ward of the Presbyterian Hospital for research study. Hypertension was first recorded 10 years before admission, with repeatedly elevated blood pressure readings up to 210/110 mm of mercury. Addison's disease developed one year before entry, as demonstrated by weakness, skin and buccal mucous membrane pigmentation and the disappearance of hypertension. The diagnosis was clinically apparent and was substantiated by the finding of repeated serum sodium values which were markedly below normal limits following salt withdrawal, calcification in the adrenal areas by x-ray and abnormally low 17-ketosteroid (2.9 mg) and neutral reducing lipid values (0.9 mg)(12)(†) in 24-hour urine specimens.