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.
Highlights
Chronic heart failure (CHF) is a diverse clinical syndrome in which impairments of ventricular filling or emptying compromise the ability of the heart to match cardiac output to metabolic demand
One study has shown that renal denervation attenuates but does not normalize the increased plasma renin activity in experimental chronic heart failure (CHF) (Witty et al, 1972), indicating that the renal nerves are partly responsible for the maladaptive activation of the systemic renin-angiotensin system (RAS)
Given the ability of the afferent renal nerves to modulate central reflexes and sympathetic outflow, we investigated the effects of renal denervation on common markers of autonomic dysfunction in the rabbit pacing model of CHF (Schiller et al, 2013)
Summary
Chronic heart failure (CHF) is a diverse clinical syndrome in which impairments of ventricular filling or emptying compromise the ability of the heart to match cardiac output to metabolic demand. This activates multiple maladaptive mechanisms such as inflammation, oxidative stress, the renin-angiotensin system (RAS), and the sympathetic nervous system (SNS), which over time contribute to disease progression (Felder et al, 2003; Tsutsui et al, 2011; Gullestad et al, 2012)
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