Abstract
Renal nerves contain afferent, sensory and efferent, sympathetic nerve fibers. In heart failure (HF) there is an increase in renal sympathetic nerve activity (RSNA), which can lead to renal vasoconstriction, increased renin release and sodium retention. These changes are thought to contribute to renal dysfunction, which is predictive of poor outcome in patients with HF. In contrast, the role of the renal afferent nerves remains largely unexplored in HF. This is somewhat surprising as there are multiple triggers in HF that have the potential to increase afferent nerve activity, including increased venous pressure and reduced kidney perfusion. Some of the few studies investigating renal afferents in HF have suggested that at least the sympatho-inhibitory reno-renal reflex is blunted. In experimentally induced HF, renal denervation, both surgical and catheter-based, has been associated with some improvements in renal and cardiac function. It remains unknown whether the effects are due to removal of the efferent renal nerve fibers or afferent renal nerve fibers, or a combination of both. Here, we review the effects of HF on renal efferent and afferent nerve function and critically assess the latest evidence supporting renal denervation as a potential treatment in HF.
Highlights
Increased Sympathetic Nerve Activity in Heart FailureThere are differential increases in sympathetic activity to individual organs in heart failure (HF), as shown by measurement of regional noradrenaline spillover in HF patients (Hasking et al, 1986)
Florey Institute of Neuroscience and Mental Health, University of Melbourne, 30 Royal Parade, Parkville, Melbourne, Specialty section: This article was submitted to Integrative Physiology, a section of the journal Frontiers in Physiology
In rabbits paced into heart failure (HF), unilateral renal denervation (RDN) prevented the reduction in renal blood flow (RBF), increase in renal vasoconstriction (RVR) and upregulation of angiotensin type-1 (AT-1) receptor expression in renal cortical blood vessels otherwise seen with HF (Clayton et al, 2011)
Summary
There are differential increases in sympathetic activity to individual organs in HF, as shown by measurement of regional noradrenaline spillover in HF patients (Hasking et al, 1986). Renal nerves in heart failure shown in HF patients and animal models of HF that the greatest increase in SNA is to the heart, with a smaller increase to the kidneys (Hasking et al, 1986; Ramchandra et al, 2009a). Large increases in RSNA have been reported in rats 4 weeks after myocardial infarction, with burst incidence increased from 35 to 47% (DiBona et al, 1988; Feng et al, 1994), and RSNA was increased from 30 to 60% of maximum in rabbits with pacing-induced HF (Liu et al, 2000, 2001). Renal noradrenaline spillover is not increased in mild HF (ejection fraction: 29%) but is significantly increased in severe HF (ejection fraction: 18%) (Rundqvist et al, 1997)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
