Sympathetic Renal Innervation and Resistant Hypertension

Hypertension in chronic renal disease and renovascular disease is often resistant to therapy. Understanding the pathogenic mechanisms responsible for hypertension in these conditions may lead to improved and more targeted therapeutic interventions. Several factors have been implicated in the pathoge...

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Main Authors: Vito M. Campese, Elaine Ku, Jeanie Park
Format: Article
Language:English
Published: Wiley 2011-01-01
Series:International Journal of Hypertension
Online Access:http://dx.doi.org/10.4061/2011/814354
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author Vito M. Campese
Elaine Ku
Jeanie Park
author_facet Vito M. Campese
Elaine Ku
Jeanie Park
author_sort Vito M. Campese
collection DOAJ
description Hypertension in chronic renal disease and renovascular disease is often resistant to therapy. Understanding the pathogenic mechanisms responsible for hypertension in these conditions may lead to improved and more targeted therapeutic interventions. Several factors have been implicated in the pathogenesis of hypertension associated with renal disease and/or renal failure. Although the role of sodium retention, total body volume expansion, and hyperactivity of the renin-angiotensin-aldosterone system (RAAS) are well recognized, increasing evidence suggests that afferent impulses from the injured kidney may increase sympathetic nervous system activity in areas of the brain involved in noradrenergic regulation of blood pressure and contribute to the development and maintenance of hypertension associated with kidney disease. Recognition of this important pathogenic factor suggests that antiadrenergic drugs should be an essential component to the management of hypertension in patients with kidney disease, particularly those who are resistant to other modalities of therapy.
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spelling doaj-art-ec900d52de684362a1bf4e82c2faea9f2025-02-03T06:13:51ZengWileyInternational Journal of Hypertension2090-03922011-01-01201110.4061/2011/814354814354Sympathetic Renal Innervation and Resistant HypertensionVito M. Campese0Elaine Ku1Jeanie Park2Division of Nephrology, USC/Keck School of Medicine, University of Southern California, 2020 Zonal Aveue, Los Angeles, CA 90033, USADivision of Nephrology, USC/Keck School of Medicine, University of Southern California, 2020 Zonal Aveue, Los Angeles, CA 90033, USARenal Division, Department of Medicine, Emory University, Atlanta, GA, USAHypertension in chronic renal disease and renovascular disease is often resistant to therapy. Understanding the pathogenic mechanisms responsible for hypertension in these conditions may lead to improved and more targeted therapeutic interventions. Several factors have been implicated in the pathogenesis of hypertension associated with renal disease and/or renal failure. Although the role of sodium retention, total body volume expansion, and hyperactivity of the renin-angiotensin-aldosterone system (RAAS) are well recognized, increasing evidence suggests that afferent impulses from the injured kidney may increase sympathetic nervous system activity in areas of the brain involved in noradrenergic regulation of blood pressure and contribute to the development and maintenance of hypertension associated with kidney disease. Recognition of this important pathogenic factor suggests that antiadrenergic drugs should be an essential component to the management of hypertension in patients with kidney disease, particularly those who are resistant to other modalities of therapy.http://dx.doi.org/10.4061/2011/814354
spellingShingle Vito M. Campese
Elaine Ku
Jeanie Park
Sympathetic Renal Innervation and Resistant Hypertension
International Journal of Hypertension
title Sympathetic Renal Innervation and Resistant Hypertension
title_full Sympathetic Renal Innervation and Resistant Hypertension
title_fullStr Sympathetic Renal Innervation and Resistant Hypertension
title_full_unstemmed Sympathetic Renal Innervation and Resistant Hypertension
title_short Sympathetic Renal Innervation and Resistant Hypertension
title_sort sympathetic renal innervation and resistant hypertension
url http://dx.doi.org/10.4061/2011/814354
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