Aldosterone Blunts Tubuloglomerular Feedback by Activating Macula Densa Mineralocorticoid Receptors
Open accessAbstract
Chronic aldosterone administration increases glomerular filtration rate, whereas inhibition of mineralocorticoid receptors (MRs) markedly attenuates glomerular hyperfiltration and hypertension associated with primary aldosteronism or obesity. However, the mechanisms by which aldosterone alters glomerular filtration rate regulation are poorly understood. In the present study, we hypothesized that aldosterone suppresses tubuloglomerular feedback (TGF) via activation of macula densa MR. First, we observed the expression of MR in macula densa cells isolated by laser capture microdissection and by immunofluorescence in rat kidneys. Second, to investigate the effects of aldosterone on TGF in vitro, we microdissected the juxtaglomerular apparatus from rabbit kidneys and perfused the afferent arteriole and distal tubule simultaneously. Under control conditions, TGF was 2.8±0.2 μm. In the presence of aldosterone (10 −8 mol/L), TGF was reduced by 50%. The effect of aldosterone to attenuate TGF was blocked by the MR antagonist eplerenone (10 −5 mol/L). Third, to investigate the effect of aldosterone on TGF in vivo, we performed micropuncture, and TGF was determined by maximal changes in stop-flow pressure P sf when tubular perfusion rate was increased from 0 to 40 nL/min. Aldosterone (10 −7 mol/L) decreased ΔP sf from 10.1±1.4 to 7.7±1.2 mm Hg. In the presence of l -NG-monomethyl arginine citrate (10 −3 mol/L), this effect was blocked. We conclude that MRs are expressed in macula densa cells and can be activated by aldosterone, which increases nitric oxide production in the macula densa and blunts the TGF response.
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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 [49]
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Amézquita, Y. C. H., Paez, L., Tovar, H., & Lizcano, C. A. R. (2023) · Revista Colombiana de Endocrinología Diabetes & Metabolismo · doi:10.53853/encr.10.2.788 · Cited by 1 · see citing works
Aldosterone and Cardiovascular Diseases
Tomaschitz, A., & Pilz, S. (2014) · Springer eBooks · doi:10.1007/978-1-4939-0509-6_12
Glomerular Hyperfiltration and Hypertension in Diabetes
Zhang, J. (2017) · Digital Commons - University of South Florida (University of South Florida)
Friedman, A. N. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-818540-7.00007-0
Implications and Management of Obesity in Kidney Disease
Friedman, A. N. (2020) · Springer eBooks · doi:10.1007/978-3-030-44858-5_12
Yoshida, Y., & Shibata, H. (2023) · Hypertension Research · doi:10.1038/s41440-023-01506-5
Sheu, J.-Y., Wu, V., & Chueh, S. (2024) · Journal of Hypertension · doi:10.1097/hjh.0000000000003611
Iwamoto, T., Hidaka, S., Iwamoto, M., & Shibata, H. (2026) · Journal of Diabetes and its Complications · doi:10.1016/j.jdiacomp.2026.109308
Function of the juxtaglomerular apparatus: control of glomerular hemodynamics and renin secretion
Schnermann, J. B., & Castrop, H. (2026) · Elsevier eBooks · doi:10.1016/b978-0-12-815389-5.00066-6
Hossain, M. R., Hurira, A., Hossain, R., Hossain, K., Alam, M. J., Rahman, M. A., Kamrujjaman, M., Sultana, N., Maraj, M. A. A., Hossain, M. A., et al. (2026) · Health Science Reports · doi:10.1002/hsr2.72922
Intrarenal Determinants of GFR Decline During Loop Diuretic Therapy
Pourafshar, N., Nam, C., Madapoosi, S., Choi, M. J., Shah, S., Pitt, B., Xiong, L., Rossignol, P., Unwin, R. J., Testani, J. M., et al. (2026) · Hypertension · doi:10.1161/hypertensionaha.126.27712
- Authors
- Fu, Y., Hall, J. E., Lu, D., Lin, L., Manning, R. D., Cheng, L., Gomez-Sanchez, C. E., Juncos, L. A., & Liu, R.
- Affiliations
- University of Mississippi Medical Center (US)
- From the Department of Physiology and Biophysics (Y.F., J.E.H., D.L., L.L., R.D.M., L.C., L.A.J., R.L.) and Division of Nephrology, Department of Medicine (L.A.J., R.L.), University of Mississippi Medical Center, Jackson, MS; Research Service (C.E.G.-S.), G.V. (Sonny) Montgomery Veterans' Affairs Medical Center, Jackson, MS.
- Venue
- Hypertension
- Published
- 2012-03
- Volume
- 59
- Issue
- 3
- Pages
- 599-606
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- PMC
- PMC3299000
- OpenAlex
- W2164322065
- Cited by
- 65
- References
- 34
- Citations by year
- 2026: 8 · 2025: 5 · 2024: 3 · 2023: 7 · 2022: 4 · 2021: 2 · 2020: 4 · 2019: 4 · 2018: 2 · 2017: 4 · 2016: 4 · 2015: 3 · 2014: 6 · 2013: 7 · 2012: 2
- FWCI
- 4.62
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL027255, HL27255, R01HL086767, P01HL051971)
- 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, tubuloglomerular feedback, macula densa, mineralocorticoid receptor, glomerular filtration rate regulation, eplerenone, nitric oxide, juxtaglomerular apparatus, primary aldosteronism, L-NG-monomethylarginine
- MeSH terms
- Aldosterone, Animals, Cells, Cultured, Feedback, Glomerular Filtration Rate, Juxtaglomerular Apparatus, Kidney Tubules, Distal, Male, Nitric Oxide, Rabbits, Rats, Sprague-Dawley, Receptors, Mineralocorticoid, Rats
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