Role of renal hemodynamics and arterial pressure in aldosterone "escape".
Abstract
This study examined the importance of changes in renal hemodynamics and renal artery pressure (RAP) in allowing the kidneys to escape from the chronic sodium-retaining effects of aldosterone (Aldo). In five dogs in which RAP was permitted to increase during Aldo infusion (14 micrograms/kg/day), sodium excretion (UNaV) and fractional sodium excretion (FENa) decreased markedly on Day 1 and then returned to control on Days 2 to 4 of Aldo infusion as RAP and glomerular filtration rate (GFR) increased 15 to 19 mm Hg and 20% to 24%, respectively, and remained near these levels during 7 days of Aldo infusion. In seven dogs in which RAP was prevented from increasing with an electronically servo-controlled aortic occluder, UNaV decreased from 256 +/- 3 to 117 +/- 9 mEq/day on the first day and remained at 70 to 80 mEq/day below sodium intake for 7 days of Aldo infusion. Cumulative sodium balance and sodium iothalamate space increased 610 +/- 39 mEq and 3729 +/- 397 ml when RAP was servo-controlled, causing ascites in most of the dogs, while mean arterial pressure did not plateau but continued to rise to 59 +/- 3 mm Hg above control after 7 days of Aldo infusion. When the servo-controller was stopped and RAP was allowed to rise while Aldo infusion was continued, GFR rose to 126% to 136% of control, FENa increased markedly, UNaV increased to 579 +/- 64 mEq/day on the first day, and the dogs returned to normal sodium balance. These data indicate that an increase in RAP, which raises GFR and FENa, is essential in allowing the kidneys to escape from the chronic sodium-retaining action of Aldo and to achieve sodium balance and a stable level of arterial pressure without severe volume expansion and ascites.
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Aldosterone activates mineralocorticoid receptors expressed on macula densa cells and increases their production of nitric oxide, which induces renal vasodilation and glomerular hyperfiltration.
“aldosterone activates MRs expressed on macula densa cells and increases their production of NO, which induces renal vasodilation and glomerular hyperfiltration48,49.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [48]
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Self-citation
- Authors
- Hall, J. E., Granger, J. P., Smith, M. J., & Premen, A. J.
- ORCID
- Hall, J E
- Venue
- Hypertension
- Published
- 1984-03
- Volume
- 6
- Issue
- 2_pt_2
- Pages
- I183-92
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- OpenAlex
- W2063605611
- Cited by
- 153
- References
- 0
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 2 · 2023: 4 · 2022: 5 · 2021: 2 · 2020: 3 · 2019: 5 · 2018: 6 · 2017: 3 · 2016: 4 · 2015: 3 · 2014: 4 · 2013: 3 · 2012: 10
- FWCI
- 2.86
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal Regulation and Hypertension
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Keywords
- aldosterone escape, renal hemodynamics, renal artery pressure, sodium retention, sodium excretion, fractional excretion of sodium, glomerular filtration rate, sodium balance, volume expansion, ascites, aortic occlusion, mean arterial pressure
- MeSH terms
- Aldosterone, Animals, Blood Pressure, Dogs, Glomerular Filtration Rate, Infusions, Parenteral, Kidney, Perfusion, Renal Circulation, Sodium
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