Glucocorticoid-induced hypertension: from mouse to man
Abstract
1. Adrenocorticotrophic hormone (ACTH) raises blood pressure in humans, sheep, rat and mouse. In rat and humans, but not sheep, the hypertension can be explained by glucocorticoid excess. 2. In both rat and humans, the hypertension is associated with a rise in cardiac output and renal vascular resistance. 3. In both rat and humans, the nitric oxide system is implicated in glucocorticoid hypertension. 4. In both rat and humans, hypertension due to naturally occurring glucocorticoids is not prevented by drugs that block classical glucocorticoid or mineralocorticoid receptors. 5. Abnormalities in glucocorticoid metabolism may contribute to some forms of 'essential' hypertension.
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Sodium and water retention secondary to adrenal secretion of glucocorticoids or mineralocorticoid hormones appears to play an important role in ACTH-induced hypertension.
“Although the mechanisms by which ACTH raises BP regulation are still unclear, sodium and water retention secondary to adrenal secretion of glucocorticoids/mineralocorticoid hormones appears to play an important role [12, 14].”
From Role of the brain melanocortins in blood pressure regulation (2017) · cites this paper as [14]
The hypertensive effects of ACTH are potentiated when renal excretory capacity is reduced by surgical removal of kidney mass.
“The importance of the renal actions of the ACTH-adrenocortical axis on BP is evident by the fact that the hypertensive effects of ACTH are potentiated when renal excretory capacity is reduced by surgical removal of kidney mass [14].”
From Role of the brain melanocortins in blood pressure regulation (2017) · cites this paper as [14]
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References 33 · Cited by 66
- Authors
- Whitworth, J. A., Schyvens, C. G., Zhang, Y., Mangos, G. J., & Kelly, J. J.
- Affiliations
- Australian National University (AU)
- Corresponding author
- Whitworth, Judith A
- Venue
- Clinical and Experimental Pharmacology and Physiology
- Publisher
- Wiley
- Published
- 2001-12-06
- Volume
- 28
- Issue
- 12
- Pages
- 993-996
- ISSN
- 0305-1870 (ISSN-L)
- 1440-1681
- OpenAlex
- W2093214567
- Cited by
- 66
- References
- 33
- Citations by year
- 2025: 1 · 2024: 1 · 2023: 4 · 2022: 3 · 2021: 2 · 2020: 3 · 2019: 1 · 2017: 3 · 2016: 1 · 2014: 2 · 2013: 6 · 2012: 1
- FWCI
- 0.49
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Clinical and Experimental Pharmacology and Physiology (publishedVersion)
- PubMed (publishedVersion)
- ANU Open Research (Australian National University) (submittedVersion)
- Funders
- Ramaciotti Foundations
- National Health and Medical Research Council
- National Medical Research Council
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal Regulation and Hypertension
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Keywords
- glucocorticoid-induced hypertension, ACTH, ACTH-induced hypertension, glucocorticoid excess, cardiac output, renal vascular resistance, nitric oxide system, glucocorticoid receptor, mineralocorticoid receptor, essential hypertension, glucocorticoid metabolism, species differences
- MeSH terms
- Adrenocorticotropic Hormone, Animals, Disease Models, Animal, Glucocorticoids, Hemodynamics, Humans, Hypertension, Nervous System, Nitric Oxide, Receptors, Steroid
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