Sympathetic nervous system activation is a hallmark of several conditions associated with an adverse prognosis, including hypertension and the metabolic syndrome. Proposed mediators of increased sympathetic drive include hyperinsulinaemia, leptin, NEFAs (non-esterified fatty acids), pro-inflammatory cytokines, baroreflex impairment and others. The role of NEFAs appears to be of particular importance given the increased levels observed in human obesity and the experimental results linking the NEFA-induced pressor response to sympathetic activation. Findings from human studies have yielded conflicting results with regards to a sympathetically mediated association between NEFAs and elevated arterial blood pressure. In the present issue of Clinical Science, Florian and Pawelczyk present some interesting results obtained from a small number of healthy normotensive lean volunteers who were exposed to NEFA infusion and cardiovascular and sympathetic monitoring using state of the art methodology that appears to be in support of such a link. However, several methodological and conceptual considerations need to be taken into account when interpreting the results from this study. Put into perspective, the case for a substantial sympathetically mediated pressor response to NEFA infusion does not appear to be a very strong one.
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January 2010
Commentary|
October 02 2009
Central sympathetic outflow to skeletal muscle: the major link between non-esterified fatty acids and elevated blood pressure?
Markus Schlaich
1Neurovascular Hypertension and Kidney Disease Laboratory, Alfred and Baker Hypertension Network, Baker IDI Heart and Diabetes Institute, Melbourne, VIC 8008, Australia
Correspondence: Associate Professor Markus Schlaich (email markus.schlaich@bakeridi.edu.au).
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Clin Sci (Lond) (2010) 118 (1): 43–45.
Article history
Received:
July 09 2009
Accepted:
July 13 2009
Accepted Manuscript online:
July 13 2009
Citation
Markus Schlaich; Central sympathetic outflow to skeletal muscle: the major link between non-esterified fatty acids and elevated blood pressure?. Clin Sci (Lond) 1 January 2010; 118 (1): 43–45. doi: https://doi.org/10.1042/CS20090369
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