TY - JOUR
T1 - Sympatho-renal axis in chronic disease
AU - Sobotka, Paul
AU - Mahfoud, Felix
AU - Schlaich, Markus
AU - Hoppe, Uta
AU - Bohm, Michael
AU - Krum, Henry
PY - 2011
Y1 - 2011
N2 - 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 kidneya??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
sympatheticsa??insulin resistance, heart failure, congestion,
diuretic resistance, and cardiorenal disorders.
AB - 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 kidneya??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
sympatheticsa??insulin resistance, heart failure, congestion,
diuretic resistance, and cardiorenal disorders.
UR - http://www.springerlink.com/content/qr32v874682mx2l0/fulltext.pdf
U2 - 10.1007/s00392-011-0335-y
DO - 10.1007/s00392-011-0335-y
M3 - Article
SN - 1861-0684
VL - 100
SP - 1049
EP - 1057
JO - Clinical Research in Cardiology
JF - Clinical Research in Cardiology
IS - 12
ER -