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SODIUM STATUS, CORTICOSTEROID METABOLISM AND BLOOD PRESSURE IN NORMAL HUMAN SUBJECTS AND IN A PATIENT WITH ABNORMAL SALT APPETITE
Author(s) -
Ingram Mary C,
Wallace A Michael,
Collier Andrew,
Fraser Robert,
McConnell John
Publication year - 1996
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1996.tb02744.x
Subject(s) - endocrinology , medicine , aldosterone , plasma renin activity , blood pressure , renin–angiotensin system , appetite , essential hypertension , sodium , metabolite , corticosteroid , urinary system , angiotensin ii , mineralocorticoid , metabolism , chemistry , organic chemistry
SUMMARY 1. A patient with severe hypertension was found to have mildly impaired 11β‐hydroxysteroid dehydrogenase (11β‐HSD) activity on the basis of urinary steroid metabolite ratios, low plasma aldosterone, angiotensin II and renin levels and marginally low levels of plasma potassium. 2. The patient also had a compulsively high salt intake. 3. We tested the hypothesis that high salt intake may affect 11β‐HSD activity. 4. High salt intake in normal subjects did not significantly alter either blood pressure or 11β‐HSD activity. 5. We suggest that the potentially small hypertensive effect of the partial enzyme deficiency in our patient, also reported in patients with essential hypertension, has been markedly amplified by the very high salt intake.