Mineralocorticoid activity of 16β-hydroxydehydroepiandrosterone and related steroids

Celso Gomez-Sanchez, O. Bryan Holland, John R. Higgins, Reese Mathieu, G. Michael Gruber, Leon Milewich, Norman M. Kaplan

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

16β-Hydroxydehydroepiandrosterone (16β-OH-DHEA) and related C19-steroids have recently been reported to be etiologic in low-renin essential hypertension. The mineralocorticoid potency of 16β-OH-DHEA and several C19-steroids (16-oxo-A-diol, 16-oxo-testosterone, 16β-OH-epiandrosterone, 5-androstene-3β, 16β, 17β-triol, 16β-OH-testosterone, 18-OH-DHEA, and 16α-OH-DHEA) were investigated in two different rat bioassay systems under a variety of experimental conditions. In all but one instance, only negligible mineralocorticoid activity was observed, usually less than 0.1 per cent that of aldosterone. Since 16β-OH-DHEA has negligible mineralocorticoid activity in the rat bioassay and the toad bladder assay (as reported by others), does not cause hypertension when injected chronically into the rat, and does not displace aldosterone from its renal receptors, it appears unlikely to be etiologic in low-renin essential hypertension. On the other hand, when 16-oxo-testosterone was injected intraperitoneally instead of subcutaneously, it demonstrated a slight increase in mineralocorticoid activity (from < 0.1 per cent to 0.2 per cent) which equaled that of 18-hydroxydeoxycorticosterone (18-OH-DOC) injected subcutaneously. Thus, the possibility remains that 16-oxo-testosterone or a closely related metabolite may have sufficient mineralocorticoid activity to be involved in certain forms of hypertension in man.

Original languageEnglish (US)
Pages (from-to)571-577
Number of pages7
JournalThe Journal of Laboratory and Clinical Medicine
Volume88
Issue number4
StatePublished - 1976

Fingerprint

Mineralocorticoids
Steroids
Dehydroepiandrosterone
Testosterone
Rats
Bioassay
Aldosterone
Renin
Biological Assay
Androsterone
Hypertension
hydroxide ion
16-hydroxydehydroepiandrosterone
Metabolites
Anura
Assays
Urinary Bladder
Kidney

ASJC Scopus subject areas

  • Medicine(all)
  • Pathology and Forensic Medicine

Cite this

Gomez-Sanchez, C., Holland, O. B., Higgins, J. R., Mathieu, R., Gruber, G. M., Milewich, L., & Kaplan, N. M. (1976). Mineralocorticoid activity of 16β-hydroxydehydroepiandrosterone and related steroids. The Journal of Laboratory and Clinical Medicine, 88(4), 571-577.

Mineralocorticoid activity of 16β-hydroxydehydroepiandrosterone and related steroids. / Gomez-Sanchez, Celso; Holland, O. Bryan; Higgins, John R.; Mathieu, Reese; Gruber, G. Michael; Milewich, Leon; Kaplan, Norman M.

In: The Journal of Laboratory and Clinical Medicine, Vol. 88, No. 4, 1976, p. 571-577.

Research output: Contribution to journalArticle

Gomez-Sanchez, C, Holland, OB, Higgins, JR, Mathieu, R, Gruber, GM, Milewich, L & Kaplan, NM 1976, 'Mineralocorticoid activity of 16β-hydroxydehydroepiandrosterone and related steroids', The Journal of Laboratory and Clinical Medicine, vol. 88, no. 4, pp. 571-577.
Gomez-Sanchez C, Holland OB, Higgins JR, Mathieu R, Gruber GM, Milewich L et al. Mineralocorticoid activity of 16β-hydroxydehydroepiandrosterone and related steroids. The Journal of Laboratory and Clinical Medicine. 1976;88(4):571-577.
Gomez-Sanchez, Celso ; Holland, O. Bryan ; Higgins, John R. ; Mathieu, Reese ; Gruber, G. Michael ; Milewich, Leon ; Kaplan, Norman M. / Mineralocorticoid activity of 16β-hydroxydehydroepiandrosterone and related steroids. In: The Journal of Laboratory and Clinical Medicine. 1976 ; Vol. 88, No. 4. pp. 571-577.
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abstract = "16β-Hydroxydehydroepiandrosterone (16β-OH-DHEA) and related C19-steroids have recently been reported to be etiologic in low-renin essential hypertension. The mineralocorticoid potency of 16β-OH-DHEA and several C19-steroids (16-oxo-A-diol, 16-oxo-testosterone, 16β-OH-epiandrosterone, 5-androstene-3β, 16β, 17β-triol, 16β-OH-testosterone, 18-OH-DHEA, and 16α-OH-DHEA) were investigated in two different rat bioassay systems under a variety of experimental conditions. In all but one instance, only negligible mineralocorticoid activity was observed, usually less than 0.1 per cent that of aldosterone. Since 16β-OH-DHEA has negligible mineralocorticoid activity in the rat bioassay and the toad bladder assay (as reported by others), does not cause hypertension when injected chronically into the rat, and does not displace aldosterone from its renal receptors, it appears unlikely to be etiologic in low-renin essential hypertension. On the other hand, when 16-oxo-testosterone was injected intraperitoneally instead of subcutaneously, it demonstrated a slight increase in mineralocorticoid activity (from < 0.1 per cent to 0.2 per cent) which equaled that of 18-hydroxydeoxycorticosterone (18-OH-DOC) injected subcutaneously. Thus, the possibility remains that 16-oxo-testosterone or a closely related metabolite may have sufficient mineralocorticoid activity to be involved in certain forms of hypertension in man.",
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N2 - 16β-Hydroxydehydroepiandrosterone (16β-OH-DHEA) and related C19-steroids have recently been reported to be etiologic in low-renin essential hypertension. The mineralocorticoid potency of 16β-OH-DHEA and several C19-steroids (16-oxo-A-diol, 16-oxo-testosterone, 16β-OH-epiandrosterone, 5-androstene-3β, 16β, 17β-triol, 16β-OH-testosterone, 18-OH-DHEA, and 16α-OH-DHEA) were investigated in two different rat bioassay systems under a variety of experimental conditions. In all but one instance, only negligible mineralocorticoid activity was observed, usually less than 0.1 per cent that of aldosterone. Since 16β-OH-DHEA has negligible mineralocorticoid activity in the rat bioassay and the toad bladder assay (as reported by others), does not cause hypertension when injected chronically into the rat, and does not displace aldosterone from its renal receptors, it appears unlikely to be etiologic in low-renin essential hypertension. On the other hand, when 16-oxo-testosterone was injected intraperitoneally instead of subcutaneously, it demonstrated a slight increase in mineralocorticoid activity (from < 0.1 per cent to 0.2 per cent) which equaled that of 18-hydroxydeoxycorticosterone (18-OH-DOC) injected subcutaneously. Thus, the possibility remains that 16-oxo-testosterone or a closely related metabolite may have sufficient mineralocorticoid activity to be involved in certain forms of hypertension in man.

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