CORTISOL METABOLISM IN HYPERTENSIVE PATIENTS WHO DO AND DO NOT DEVELOP HYPOKALEMIA FROM DIURETICS

Citation
Dl. Santini et al., CORTISOL METABOLISM IN HYPERTENSIVE PATIENTS WHO DO AND DO NOT DEVELOP HYPOKALEMIA FROM DIURETICS, American journal of hypertension, 8(5), 1995, pp. 516-519
Citations number
NO
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
08957061
Volume
8
Issue
5
Year of publication
1995
Part
1
Pages
516 - 519
Database
ISI
SICI code
0895-7061(1995)8:5<516:CMIHPW>2.0.ZU;2-5
Abstract
Deficiency of 11 beta-hydroxysteroid dehydrogenase causes hypertension and hypokalemia. To test whether hypertensive patients who develop hy pokalemia when treated with diuretics have low levels of activity of t his enzyme as a metabolic predisposition to the development of hypokal emia, we measured urinary cortisone, cortisol, tetrahydrocortisol, tet rahydrocortisone, and creatinine in 42 hypertensive patients who eithe r did or did not become hypokalemic on hydrochlorothiazide. The mean r atios of cortisone to cortisol, tetrahydrocortisone to tetrahydrocorti sol, tetrahydrocortisol to cortisol, and cortisol to creatinine did no t differ between the two groups. We conclude that hypertensives who de velop hypokalemia on diuretics do not have low activity of this enzyme . They also do not appear to have low ring A reduction or higher corti sol secretion rates compared with hypertensives who do not develop hyp okalemia. We failed to find a metabolic predisposition to the developm ent of hypokalemia by diuretic treatment.