Abstract
Activation of the sympathetic nervous system (SNS) has been identified as a key pathophysiological feature involved in the initiation, progression but also prognosis of most cardiometabolic disorders (chronic heart failure or kidney disease, coronary heart disease, obesity, diabetes, etc.), among them hypertension (HTN). This has been established through studies recording SNS activation at systemic and local levels using different techniques to measure SNS outflow to various organs. Mechanisms leading to SNS activation are heterogeneous varying from central activation to reflex-mediated sympathoexcitation (or lack of sympathoinhibition).
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- BP:
-
Blood pressure
- CGRP:
-
Calcitonin gene-related peptide
- CHF:
-
Congestive heart failure
- GFR:
-
Glomerular filtration rate
- HR:
-
Heart rate
- HTN:
-
Hypertension
- JGC:
-
Juxtaglomerular granular cells
- MSNA:
-
Muscle sympathetic nerve activity
- NOx:
-
Nitrogen oxide
- RBF:
-
Renal blood flow
- RDN:
-
Renal denervation
- SHR:
-
Spontaneously hypertensive rats
- SNA:
-
Sympathetic nerve activity
- SNS:
-
Sympathetic nervous system
- SP:
-
Surfactant protein
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Pathak, A., Honton, B., Lobo, M. (2016). Pathophysiology of Renal Sympathetic Denervation (RSDN). In: Tsioufis, C., Schmieder, R., Mancia, G. (eds) Interventional Therapies for Secondary and Essential Hypertension. Updates in Hypertension and Cardiovascular Protection. Springer, Cham. https://doi.org/10.1007/978-3-319-34141-5_12
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