Cultural advice

The Australian National University acknowledges, celebrates and pays our respects to the Ngunnawal and Ngambri people of the Canberra region and to all First Nations Australians on whose traditional lands we meet and work, and whose cultures are among the oldest continuing cultures in human history.

Aboriginal and Torres Strait Islander peoples are advised that ANU Library collections may include images, names, voices, and other representations of deceased persons.

Material in the collection may contain terms, language or views that reflect the period in which the item was created and may be considered inappropriate today.

Role of erythropoietin in cortisol-induced hypertension

Loading...
Thumbnail Image

Date

Authors

Kelly, John J
Martin, Allison
Whitworth, Judith

Journal Title

Journal ISSN

Volume Title

Publisher

Nature Publishing Group

Abstract

The mechanism of cortisol-induced hypertension remains unknown. We investigated a possible role of erythropoietin (EPO) as a mediator of hypertension in healthy male subjects treated with cortisol. In study 1, blood pressure (BP) and serum EPO concentrations were measured on alternate days in nine subjects treated with 80 mg of cortisol per day for 5 days. In Study 2 the same parameters were measured in eight subjects randomised to cortisol (80 mg/day) or placebo and 10 subjects randomised to cortisol (200 mg/day) or placebo for 5 days. In study 1, cortisol caused a significant increase in systolic BP (SBP) (115 ± 2 vs 126 ± 2 mm Hg, control vs day 5, P < 0.001) and serum EPO concentrations (14.5 ± 2.7 vs 24.3 ± 2.7 mU/mL, P < 0.001). In Study 2 both doses of cortisol increased SBP (118 ± 2 vs 113 ± 2 mm Hg, 80 mg cortisol vs placebo, P < 0.05 and 129 ± 3 vs 113 ± 2 mm Hg, 200 mg cortisol vs placebo, P < 0.001). Serum EPO concentrations were significantly increased at 200 mg cortisol (25.2 ± 11.9 vs 15.9 ± 3.5 mU/mL, P < 0.01) but not 80 mg cortisol (21.3 ± 2.9 vs 14.9 ± 3.1 mU/mL). In the 200 mg group there was a positive correlation between the change in SBP and the change in serum EPO concentration (r2 = 0.43, P < 0.05). These results point to a possible role for EPO as the mediator of cortisol-induced hypertension.

Description

Citation

Source

Journal of Human Hypertension

Book Title

Entity type

Access Statement

License Rights

DOI

Restricted until

abcd