Abstract
Heart failure (HF) is a serious debilitating condition with poor survival rates and an increasing level of prevalence. HF is associated with an increase in renal norepinephrine (NE) spillover, which is an independent predictor of mortality in HF patients. The excessive sympatho-excitation that is a hallmark of HF has long-term effects that contribute to disease progression. An increase in directly recorded renal sympathetic nerve activity (RSNA) has also been recorded in animal models of HF. This review will focus on the mechanisms controlling sympathetic nerve activity (SNA) to the kidney during normal conditions and alterations in these mechanisms during HF. In particular the roles of afferent reflexes and central mechanisms will be discussed.
Highlights
Heart failure (HF) is a complex syndrome, arising secondary to a wide range of cardiac structural and functional abnormalities, with the manifestations being shortness of breath, fatigue, exercise intolerance, and oedema
Understanding the role of renal sympathetic nerve activity (RSNA) in HF is difficult in humans where measurement is indirect at best
Evidence does suggest that deterioration in cardiac function in HF is closely associated with elevations in RSNA, it would appear that increased NE spillover only becomes significant once the ejection fraction is reduced below 30%
Summary
Reviewed by: Kenju Miki, Nara Women’s University, Japan Luciana A. Specialty section: This article was submitted to Integrative Physiology, a section of the journal Frontiers in Physiology. Regulation of the renal sympathetic nerves in heart failure. Heart failure (HF) is a serious debilitating condition with poor survival rates and an increasing level of prevalence. HF is associated with an increase in renal norepinephrine (NE) spillover, which is an independent predictor of mortality in HF patients. An increase in directly recorded renal sympathetic nerve activity (RSNA) has been recorded in animal models of HF. This review will focus on the mechanisms controlling sympathetic nerve activity (SNA) to the kidney during normal conditions and alterations in these mechanisms during HF. In particular the roles of afferent reflexes and central mechanisms will be discussed
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