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Hypothetical model of central sympathetic dysregulation in HF; hypothesis-generating and requires experimental validation before research or clinical translation.
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 central 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.
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Weiss et al. (2002) studied this question.
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