Limits...
The renal nerves in chronic heart failure: efferent and afferent mechanisms.

Schiller AM, Pellegrino PR, Zucker IH - Front Physiol (2015)

Bottom Line: Renal denervation in CHF also reduced physiological markers of autonomic dysfunction including an improvement in arterial baroreflex function, heart rate variability, and decreased resting cardiac sympathetic tone.Taken together, the renal sympathetic nerves are necessary in the pathogenesis of CHF via both efferent and afferent mechanisms.Additional investigation is warranted to fully understand the role of these nerves and their role as a therapeutic target in CHF.

View Article: PubMed Central - PubMed

Affiliation: Cellular and Integrative Physiology, University of Nebraska Medical Center Omaha, NE, USA.

ABSTRACT
The function of the renal nerves has been an area of scientific and medical interest for many years. The recent advent of a minimally invasive catheter-based method of renal denervation has renewed excitement in understanding the afferent and efferent actions of the renal nerves in multiple diseases. While hypertension has been the focus of much this work, less attention has been given to the role of the renal nerves in the development of chronic heart failure (CHF). Recent studies from our laboratory and those of others implicate an essential role for the renal nerves in the development and progression of CHF. Using a rabbit tachycardia model of CHF and surgical unilateral renal denervation, we provide evidence for both renal efferent and afferent mechanisms in the pathogenesis of CHF. Renal denervation prevented the decrease in renal blood flow observed in CHF while also preventing increases in Angiotensin-II receptor protein in the microvasculature of the renal cortex. Renal denervation in CHF also reduced physiological markers of autonomic dysfunction including an improvement in arterial baroreflex function, heart rate variability, and decreased resting cardiac sympathetic tone. Taken together, the renal sympathetic nerves are necessary in the pathogenesis of CHF via both efferent and afferent mechanisms. Additional investigation is warranted to fully understand the role of these nerves and their role as a therapeutic target in CHF.

No MeSH data available.


Related in: MedlinePlus

Efferent and afferent signaling in the development of experimental CHF. Rabbits were chronically instrumented with ventricular pacing leads, arterial pressure radiotelemeters, and renal flow probes, and underwent surgical denervation or a sham procedure (A). Induction of CHF by ventricular pacing reduced blood flow in innervated (INV) rabbits but not in denervated (DNV) rabbits (B). Modified from Clayton et al. (2011). Induction of CHF also reduced baroreflex gain and potentiated the heart rate response to metoprolol in INV but not DNV rabbits (C). Modified from Schiller et al. (2013).
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4528173&req=5

Figure 1: Efferent and afferent signaling in the development of experimental CHF. Rabbits were chronically instrumented with ventricular pacing leads, arterial pressure radiotelemeters, and renal flow probes, and underwent surgical denervation or a sham procedure (A). Induction of CHF by ventricular pacing reduced blood flow in innervated (INV) rabbits but not in denervated (DNV) rabbits (B). Modified from Clayton et al. (2011). Induction of CHF also reduced baroreflex gain and potentiated the heart rate response to metoprolol in INV but not DNV rabbits (C). Modified from Schiller et al. (2013).

Mentions: Recent studies from our laboratory investigated the role of the renal nerves in CHF in the rabbit rapid ventricular pacing model (Clayton et al., 2011; Schiller et al., 2013). The animals were chronically instrumented with ventricular pacing leads, arterial pressure radiotelemetries, and renal flow probes (Figure 1A). The kidney instrumented with a flow probe either underwent surgical denervation (DNV) or remained innervated (INV). CHF was induced over several weeks and validated by echocardiography. This model exhibits increases in renal sympathetic nerve activity (RSNA), plasma angiotensin II, and plasma norepinephrine (Mousa et al., 2008; Schiller et al., 2013), recapitulating the pathophysiology of human CHF. All studies were performed in the conscious state in rabbits that were well acclimated to the experimental procedures and environment.


The renal nerves in chronic heart failure: efferent and afferent mechanisms.

Schiller AM, Pellegrino PR, Zucker IH - Front Physiol (2015)

Efferent and afferent signaling in the development of experimental CHF. Rabbits were chronically instrumented with ventricular pacing leads, arterial pressure radiotelemeters, and renal flow probes, and underwent surgical denervation or a sham procedure (A). Induction of CHF by ventricular pacing reduced blood flow in innervated (INV) rabbits but not in denervated (DNV) rabbits (B). Modified from Clayton et al. (2011). Induction of CHF also reduced baroreflex gain and potentiated the heart rate response to metoprolol in INV but not DNV rabbits (C). Modified from Schiller et al. (2013).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4528173&req=5

Figure 1: Efferent and afferent signaling in the development of experimental CHF. Rabbits were chronically instrumented with ventricular pacing leads, arterial pressure radiotelemeters, and renal flow probes, and underwent surgical denervation or a sham procedure (A). Induction of CHF by ventricular pacing reduced blood flow in innervated (INV) rabbits but not in denervated (DNV) rabbits (B). Modified from Clayton et al. (2011). Induction of CHF also reduced baroreflex gain and potentiated the heart rate response to metoprolol in INV but not DNV rabbits (C). Modified from Schiller et al. (2013).
Mentions: Recent studies from our laboratory investigated the role of the renal nerves in CHF in the rabbit rapid ventricular pacing model (Clayton et al., 2011; Schiller et al., 2013). The animals were chronically instrumented with ventricular pacing leads, arterial pressure radiotelemetries, and renal flow probes (Figure 1A). The kidney instrumented with a flow probe either underwent surgical denervation (DNV) or remained innervated (INV). CHF was induced over several weeks and validated by echocardiography. This model exhibits increases in renal sympathetic nerve activity (RSNA), plasma angiotensin II, and plasma norepinephrine (Mousa et al., 2008; Schiller et al., 2013), recapitulating the pathophysiology of human CHF. All studies were performed in the conscious state in rabbits that were well acclimated to the experimental procedures and environment.

Bottom Line: Renal denervation in CHF also reduced physiological markers of autonomic dysfunction including an improvement in arterial baroreflex function, heart rate variability, and decreased resting cardiac sympathetic tone.Taken together, the renal sympathetic nerves are necessary in the pathogenesis of CHF via both efferent and afferent mechanisms.Additional investigation is warranted to fully understand the role of these nerves and their role as a therapeutic target in CHF.

View Article: PubMed Central - PubMed

Affiliation: Cellular and Integrative Physiology, University of Nebraska Medical Center Omaha, NE, USA.

ABSTRACT
The function of the renal nerves has been an area of scientific and medical interest for many years. The recent advent of a minimally invasive catheter-based method of renal denervation has renewed excitement in understanding the afferent and efferent actions of the renal nerves in multiple diseases. While hypertension has been the focus of much this work, less attention has been given to the role of the renal nerves in the development of chronic heart failure (CHF). Recent studies from our laboratory and those of others implicate an essential role for the renal nerves in the development and progression of CHF. Using a rabbit tachycardia model of CHF and surgical unilateral renal denervation, we provide evidence for both renal efferent and afferent mechanisms in the pathogenesis of CHF. Renal denervation prevented the decrease in renal blood flow observed in CHF while also preventing increases in Angiotensin-II receptor protein in the microvasculature of the renal cortex. Renal denervation in CHF also reduced physiological markers of autonomic dysfunction including an improvement in arterial baroreflex function, heart rate variability, and decreased resting cardiac sympathetic tone. Taken together, the renal sympathetic nerves are necessary in the pathogenesis of CHF via both efferent and afferent mechanisms. Additional investigation is warranted to fully understand the role of these nerves and their role as a therapeutic target in CHF.

No MeSH data available.


Related in: MedlinePlus