Translational medicine: the antihypertensive effect of renal denervation
Abstract
Translational medicine is concerned with the translation of research discoveries into clinical applications for the prevention, diagnosis, and treatment of human diseases. Here we briefly review the research concerning the role of the renal sympathetic nerves (efferent and afferent) in the control of renal function, with particular reference to hypertension. The accumulated evidence is compelling for a primary role of the renal innervation in the pathogenesis of hypertension. These research discoveries led to the development of a catheter-based procedure for renal denervation in human subjects. A proof-of-principle study in patients with hypertension resistant to conventional therapy has demonstrated that the procedure is safe and produces renal denervation with sustained lowering of arterial pressure.
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Renal sympathetic nerves are distributed to all levels of the nephron.
“Renal sympathetic nerves are distributed to all levels of the nephron.101,102”
From Obesity Paradox in Hypertension: Is This Because Sympathetic Activation in Obesity-Hypertension Takes a Benign Form? (2018) · cites this paper as [102]
Renal sympathetic activation is central to the pathogenesis of essential hypertension.
“Renal sympathetic activation is thought to be central to the pathogenesis of essential hypertension94–96.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [96]
Renal sympathetic denervation shifts the renal pressure-natriuresis curve to the left, promoting urinary sodium excretion and lowering blood pressure.
“Renal sympathetic denervation shifts the renal pressure-natriuresis curve to the left, promoting urinary sodium excretion and lowering of blood pressure94–98.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [96]
Renal parenchymal nociceptive sensory nerves respond to a renal injury signal by projecting to the hypothalamus to increase central sympathetic outflow.
“The first, of the renal parenchyma and bearing nociceptive receptors, respond to a renal injury signal by projecting to the hypothalamus to increase central sympathetic outflow95–99.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [96]
Three facts provided the knowledge base for the development of catheter-based renal denervation for treatment of essential hypertension: the presence of an activated renal sympathetic outflow in hypertensive patients, the blood-pressure lowering effect of surgical renal denervation in experimental models of hypertension, and the anatomy of the postganglionic renal sympathetic nerves in theirpassag
“Three facts provided the knowledge base for the development of catheter-based renal denervation for treatment of essential hypertension: 1) the presence of an activated renal sympathetic outflow in hypertensive patients, 2) the blood-pressure lowering effect of surgical renal denervation in experimental models of hypertension, and 3) the anatomy of the postganglionic renal sympathetic nerves in”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [96]
Renal denervation is invariably antihypertensive in four mammalian species (rats, dogs, rabbits, pigs).
“Why should renal denervation, in four mammalian species (rats, dogs, rabbits pigs) invariably be antihypertensive95–96”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [96]
Experimental surgical and catheter-based denervation for hypertension still works.
“Experimental surgical and catheter-based denervation for hypertension still works!”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [96]
Several clinical studies have demonstrated that renal denervation reduces blood pressure in hypertensive patients.
“Several clinical studies have demonstrated that renal denervation reduces blood pressure in hypertensive patients (1, 16, 37).”
From A mathematical model of long-term renal sympathetic nerve activity inhibition during an increase in sodium intake (2014) · cites this paper as [16]
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- Authors
- DiBona, G. F., & Esler, M.
- Affiliations
- University of Iowa (US)
- Baker Heart and Diabetes Institute (AU)
- Corresponding author
- DiBona, Gerald F.
- Venue
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
- Publisher
- American Physiological Society
- Published
- 2010-02
- Volume
- 298
- Issue
- 2
- Pages
- R245-R253
- ISSN
- 0363-6119 (ISSN-L)
- 1522-1490
- OpenAlex
- W2129162046
- Cited by
- 432
- References
- 61
- Citations by year
- 2026: 11 · 2025: 15 · 2024: 20 · 2023: 22 · 2022: 10 · 2021: 18 · 2020: 18 · 2019: 24 · 2018: 17 · 2017: 24 · 2016: 28 · 2015: 34 · 2014: 68 · 2013: 55 · 2012: 36
- FWCI
- 3.41
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Keywords
- renal denervation, hypertension, renal sympathetic nerves, renal innervation, renal function, resistant hypertension, catheter-based procedures, antihypertensive effect, translational medicine
- MeSH terms
- Animals, Glomerular Filtration Rate, Humans, Hypertension, Kidney, Renal Circulation, Renin, Sympathectomy, Sympathetic Nervous System, Translational Research, Biomedical
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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