TY - JOUR
T1 - Modifications to central neural circuitry during heart failure
AU - Weiss, M. L.
AU - Kenney, M. J.
AU - Musch, T. I.
AU - Patel, K. P.
PY - 2003
Y1 - 2003
N2 - Aim: During heart failure (HF), excess sodium retention is triggered by increased plasma renin-angiotensin-aldosterone activity and increased basal sympathetic nerve discharge (SND). Enhanced basal SND in the renal nerves plays a role in sodium retention. Therefore, as a hypothetical model for the central sympathetic control pathways that are dysregulated as a consequence of HF, the cental neural pathways regulating the sympathetic motor output to the kidney are reviewed in the context of their role during HF. Conclusion: From these findings, a model of the neuroanatomical circuitry that may be affected during HF is constructed.
AB - Aim: During heart failure (HF), excess sodium retention is triggered by increased plasma renin-angiotensin-aldosterone activity and increased basal sympathetic nerve discharge (SND). Enhanced basal SND in the renal nerves plays a role in sodium retention. Therefore, as a hypothetical model for the central sympathetic control pathways that are dysregulated as a consequence of HF, the cental neural pathways regulating the sympathetic motor output to the kidney are reviewed in the context of their role during HF. Conclusion: From these findings, a model of the neuroanatomical circuitry that may be affected during HF is constructed.
KW - Brain renin-angiotension system
KW - Central autonomic control
KW - Kidney
KW - Myocardial infarction
KW - Sympathetic nervous system
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U2 - 10.1046/j.1365-201X.2003.01047.x
DO - 10.1046/j.1365-201X.2003.01047.x
M3 - Article
C2 - 12492779
AN - SCOPUS:0037227240
VL - 177
SP - 57
EP - 67
JO - Acta Physiologica Scandinavica
JF - Acta Physiologica Scandinavica
SN - 0001-6772
IS - 1
ER -