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Cited by 144Blood Pressure and Hypertension StudiesRenin-Angiotensin System StudiesVagus Nerve Stimulation Research

Resting Afferent Renal Nerve Discharge and Renal Inflammation: Elucidating the Role of Afferent and Efferent Renal Nerves in Deoxycorticosterone Acetate Salt Hypertension

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Banek, Christopher T., Knuepfer, Mark M., Foss, Jason D., Fiege, Jessica K., Asirvatham-Jeyaraj, Ninitha, Van Helden, Dusty, Shimizu, Yoji, Osborn, John W.·2016·Hypertension
DOI 10.1161/hypertensionaha.116.07850PMC PMC5159336
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Abstract

Renal sympathetic denervation (RDNx) has emerged as a novel therapy for hypertension; however, the therapeutic mechanisms remain unclear. Efferent renal sympathetic nerve activity has recently been implicated in trafficking renal inflammatory immune cells and inflammatory chemokine and cytokine release. Several of these inflammatory mediators are known to activate or sensitize afferent nerves. This study aimed to elucidate the roles of efferent and afferent renal nerves in renal inflammation and hypertension in the deoxycorticosterone acetate (DOCA) salt rat model. Uninephrectomized male Sprague–Dawley rats (275–300 g) underwent afferent-selective RDNx (n=10), total RDNx (n=10), or Sham (n=10) and were instrumented for the measurement of mean arterial pressure and heart rate by radiotelemetry. Rats received 100-mg DOCA (SC) and 0.9% saline for 21 days. Resting afferent renal nerve activity in DOCA and vehicle animals was measured after the treatment protocol. Renal tissue inflammation was assessed by renal cytokine content and T-cell infiltration and activation. Resting afferent renal nerve activity, expressed as a percent of peak afferent nerve activity, was substantially increased in DOCA than in vehicle (35.8±4.4 versus 15.3±2.8 %Amax). The DOCA–Sham hypertension (132±12 mm Hg) was attenuated by ≈50% in both total RDNx (111±8 mm Hg) and afferent-selective RDNx (117±5 mm Hg) groups. Renal inflammation induced by DOCA salt was attenuated by total RDNx and unaffected by afferent-selective RDNx. These data suggest that afferent renal nerve activity may mediate the hypertensive response to DOCA salt, but inflammation may be mediated primarily by efferent renal sympathetic nerve activity. Also, resting afferent renal nerve activity is elevated in DOCA salt rats, which may highlight a crucial neural mechanism in the development and maintenance of hypertension.

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  • Preclinical studies have identified a previously underappreciated role of afferent renal nerves in hypertension and chronic kidney disease.

    “Preclinical studies have now identified a previously underappreciated role of afferent renal nerves in the development of hypertension and chronic kidney disease (CKD)5,20–22.”

    From Renal nerves in physiology, pathophysiology and interoception (2025) · cites this paper as [22]

    The Discussion (page not available in our copy) concludes that afferent renal nerves contribute to the development of DOCA-salt hypertension in rats. It also discusses hypertension following renal injury and in chronic renal failure, but does not establish a role for afferent nerves in the development of chronic kidney disease itself. (LLM, conf=0.87)

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  • Afferent renal denervation is as effective as total renal denervation for hypertension in DOCA-salt and 2K1C models.

    “We and others have demonstrated that ARDN is as efficacious as TRDN for the treatment of hypertension in the DOCA-salt rat22,76 and 2K1C models5,20.”

    From Renal nerves in physiology, pathophysiology and interoception (2025) · cites this paper as [22]

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Authors
Banek, C. T., Knuepfer, M. M., Foss, J. D., Fiege, J. K., Asirvatham-Jeyaraj, N., Van Helden, D., Shimizu, Y., & Osborn, J. W.
Affiliations
  • University of Minnesota (US)
  • From the Department of Integrative Biology and Physiology (C.T.B., J.D.F., N.A.-J., D.V.H., J.W.O.) and Department of Laboratory Medicine and Pathology (J.K.F., Y.S), University of Minnesota Medical School, Minneapolis; and Department of Pharmacology and Physiology, Saint Louis University School of Medicine, MO (M.M.K.).
ORCID
Venue
Hypertension
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2016-12
Volume
68
Issue
6
Pages
1415-1423
ISSN
  • 0194-911X (ISSN-L)
  • 1524-4563
DOI
10.1161/hypertensionaha.116.07850
PMC
PMC5159336
OpenAlex
W2528919820
Cited by
144
References
44
Citations by year
2026: 14 · 2025: 15 · 2024: 21 · 2023: 17 · 2022: 9 · 2021: 20 · 2020: 15 · 2019: 16 · 2018: 11 · 2017: 6
FWCI
9.07
Type
journal article
Language
en
Open access
Locations
  • Hypertension (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Heart, Lung, and Blood Institute (R01HL116476, T32HL007741)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
  • Life Sciences › Neuroscience › Neurology › Vagus Nerve Stimulation Research
Keywords
renal denervation, renal inflammation, DOCA-salt hypertension, T cell infiltration, chemokines, immune cell trafficking, unilateral nephrectomy, renal innervation
MeSH terms
Animals, Disease Models, Animal, Hypertension, Kidney, Male, Nephritis, Neurons, Afferent, Random Allocation, Rest, Role, Sympathectomy, Sympathetic Nervous System, Rats, Sprague-Dawley, Rats, Desoxycorticosterone Acetate

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