Sympatho-renal axis in chronic disease

Paul A. Sobotka, Felix Mahfoud, Markus P. Schlaich, Uta C. Hoppe, Michael Böhm, Henry Krum

Research output: Contribution to journalReview article

143 Citations (Scopus)

Abstract

Essential hypertension, insulin resistance, heart failure, congestion, diuretic resistance, and functional renal disease are all characterized by excessive central sympathetic drive. The contribution of the kidney's somatic afferent nerves, as an underlying cause of elevated central sympathetic drive, and the consequences of excessive efferent sympathetic signals to the kidney itself, as well as other organs, identify the renal sympathetic nerves as a uniquely logical therapeutic target for diseases linked by excessive central sympathetic drive. Clinical studies of renal denervation in patients with resistant hypertension using an endovascular radiofrequency ablation methodology have exposed the sympathetic link between these conditions. Renal denervation could be expected to simultaneously affect blood pressure, insulin resistance, sleep disorders, congestion in heart failure, cardiorenal syndrome and diuretic resistance. The striking epidemiologic evidence for coexistence of these disorders suggests common causal pathways. Chronic activation of the sympathetic nervous system has been associated with components of the metabolic syndrome, such as blood pressure elevation, obesity, dyslipidemia, and impaired fasting glucose with hyperinsulinemia. Over 50% of patients with essential hypertension are hyperinsulinemic, regardless of whether they are untreated or in a stable program of treatment. Insulin resistance is related to sympathetic drive via a bidirectional mechanism. In this manuscript, we review the data that suggests that selective impairment of renal somatic afferent and sympathetic efferent nerves in patients with resistant hypertension both reduces markers of central sympathetic drive and favorably impacts diseases linked through central sympathetics-insulin resistance, heart failure, congestion, diuretic resistance, and cardiorenal disorders.

Original languageEnglish
Pages (from-to)1049-1057
Number of pages9
JournalClinical Research in Cardiology
Volume100
Issue number12
DOIs
Publication statusPublished - Dec 2011
Externally publishedYes

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Chronic Disease
Kidney
Insulin Resistance
Diuretics
Heart Failure
Denervation
Cardio-Renal Syndrome
Blood Pressure
Hypertension
Sympathetic Nervous System
Hyperinsulinism
Dyslipidemias
Fasting
Obesity
Drive
Glucose
Therapeutics
Essential Hypertension

Cite this

Sobotka, P. A., Mahfoud, F., Schlaich, M. P., Hoppe, U. C., Böhm, M., & Krum, H. (2011). Sympatho-renal axis in chronic disease. Clinical Research in Cardiology, 100(12), 1049-1057. https://doi.org/10.1007/s00392-011-0335-y
Sobotka, Paul A. ; Mahfoud, Felix ; Schlaich, Markus P. ; Hoppe, Uta C. ; Böhm, Michael ; Krum, Henry. / Sympatho-renal axis in chronic disease. In: Clinical Research in Cardiology. 2011 ; Vol. 100, No. 12. pp. 1049-1057.
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Sobotka, PA, Mahfoud, F, Schlaich, MP, Hoppe, UC, Böhm, M & Krum, H 2011, 'Sympatho-renal axis in chronic disease' Clinical Research in Cardiology, vol. 100, no. 12, pp. 1049-1057. https://doi.org/10.1007/s00392-011-0335-y

Sympatho-renal axis in chronic disease. / Sobotka, Paul A.; Mahfoud, Felix; Schlaich, Markus P.; Hoppe, Uta C.; Böhm, Michael; Krum, Henry.

In: Clinical Research in Cardiology, Vol. 100, No. 12, 12.2011, p. 1049-1057.

Research output: Contribution to journalReview article

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T1 - Sympatho-renal axis in chronic disease

AU - Sobotka, Paul A.

AU - Mahfoud, Felix

AU - Schlaich, Markus P.

AU - Hoppe, Uta C.

AU - Böhm, Michael

AU - Krum, Henry

PY - 2011/12

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N2 - Essential hypertension, insulin resistance, heart failure, congestion, diuretic resistance, and functional renal disease are all characterized by excessive central sympathetic drive. The contribution of the kidney's somatic afferent nerves, as an underlying cause of elevated central sympathetic drive, and the consequences of excessive efferent sympathetic signals to the kidney itself, as well as other organs, identify the renal sympathetic nerves as a uniquely logical therapeutic target for diseases linked by excessive central sympathetic drive. Clinical studies of renal denervation in patients with resistant hypertension using an endovascular radiofrequency ablation methodology have exposed the sympathetic link between these conditions. Renal denervation could be expected to simultaneously affect blood pressure, insulin resistance, sleep disorders, congestion in heart failure, cardiorenal syndrome and diuretic resistance. The striking epidemiologic evidence for coexistence of these disorders suggests common causal pathways. Chronic activation of the sympathetic nervous system has been associated with components of the metabolic syndrome, such as blood pressure elevation, obesity, dyslipidemia, and impaired fasting glucose with hyperinsulinemia. Over 50% of patients with essential hypertension are hyperinsulinemic, regardless of whether they are untreated or in a stable program of treatment. Insulin resistance is related to sympathetic drive via a bidirectional mechanism. In this manuscript, we review the data that suggests that selective impairment of renal somatic afferent and sympathetic efferent nerves in patients with resistant hypertension both reduces markers of central sympathetic drive and favorably impacts diseases linked through central sympathetics-insulin resistance, heart failure, congestion, diuretic resistance, and cardiorenal disorders.

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KW - Congestion

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KW - Hypertension

KW - Insulin resistance

KW - Renal denervation

KW - Sleep apnea

KW - Sympathetic nervous system

KW - Symplicity HTN-2

KW - Tachycardiac arrhythmias

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U2 - 10.1007/s00392-011-0335-y

DO - 10.1007/s00392-011-0335-y

M3 - Review article

VL - 100

SP - 1049

EP - 1057

JO - Clinical Research in Cardiology

JF - Clinical Research in Cardiology

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Sobotka PA, Mahfoud F, Schlaich MP, Hoppe UC, Böhm M, Krum H. Sympatho-renal axis in chronic disease. Clinical Research in Cardiology. 2011 Dec;100(12):1049-1057. https://doi.org/10.1007/s00392-011-0335-y