Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The isolation of 18-hydroxycortisol and 18-oxocortisol was recently described. These steroids have been shown to be excreted in exaggerated quantities in patients with primary aldosteronism, with adrenal adenomas and in glucocorticoid suppressible aldosteronism. We report the measurement of both steroids in the urine of patients with essential hypertension. 18-Oxocortisol excretion did not differ in patients with normal renin essential hypertension (0.7 +/- 0.7 micrograms/24 h), low renin essential hypertension (0.7 +/- 0.5 micrograms/24 h) and normal individuals (1.2 +/- 0.9 micrograms/24 h). Patients with normal renin hypertension excreted 54 +/- 43 micrograms/24 h of 18-hydroxycortisol, those with low renin essential hypertension excreted 58 +/- 54 micrograms/24 h, and normal individuals excreted 63 +/- 36 micrograms/24 h. Three of the low renin and one of the normal renin hypertensive subjects excreted greater quantities of 18-hydroxycortisol than the upper limit of normal, but all excreted normal quantities of 18-oxocortisol. As 18-hydroxycortisol is inactive, the meaning of this elevated excretion is unclear, but it may be a marker of an adrenal enzymatic abnormality which may be playing a more direct role in hypertension.
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PMID:Role of 18-hydroxylated cortisols in hypertension. 332 May 70

A radioimmunoassay procedure for the measurement of urinary 18-oxocortisol was developed. The antibody was raised against 18-oxocortisol 3-carboxymethyloxime-BSA and had relatively high specificity, except for aldosterone (26.3%). The RIA required a preliminary HPLC purification using a Lichrosorb diol column eluted with toluene:acetonitrile:isopropanol:acetic acid (83:11.9:5.1:0.01). The eluate portion corresponding to 18-oxocortisol was evaporated and subjected to RIA. The RIA procedure had an intraassay variability of 11% when using a pool containing 10.8 micrograms/24 hr (n = 6) and 17% with a pool containing 3.28 micrograms/24 hr. The interassay variability was 11% (n = 4). The recovery of added 18-oxocortisol was 90 +/- 10%. The urinary excretion of 18-oxocortisol in 22 white normal subjects was 3.26 +/- 1.98 (SD) micrograms/24 hr (range 0.8 to 7.1 micrograms/24 hr). The mean excretion of 18-oxocortisol in 4 patients with glucocorticoid-suppressible aldosteronism (GSA) was 38.6 micrograms/24 hr (range 25.5 to 54.6 micrograms/24 hr). The excretion of 18-oxocortisol in 3 patients with adenomas producing primary aldosteronism (APA) varied between 11.1 to 17.3 micrograms/24 hr and in 3 patients with idiopathic aldosteronism (IA) varied between 2.5 to 10.6 micrograms/24 hr. 18-Oxocortisol excretion is increased markedly in the urine of patients with GSA: what role this relatively weak mineralocorticoid plays in the pathogenesis of their hypertension is unknown. Its elevation is probably a reflection of a postulated lack of involution of the 18-methyloxidase in the inner layers of the adrenal.
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PMID:Elevated urinary excretion of 18-oxocortisol in glucocorticoid-suppressible aldosteronism. 648 Aug 7