Cardiopulmonary Baroreflex Control of Renal Sympathetic Nerve Activity Is Impaired in Dogs With Left Ventricular...

Area of Science:

• Cardiovascular Physiology
• Neurocardiology
• Heart Failure Pathophysiology

Background:

• Neurohormonal system activation is a key driver of heart failure (HF) progression.
• Mechanisms underlying neurohormonal activation in HF remain incompletely understood.
• Vagal cardiopulmonary baroreflex regulation of sympathetic nerve activity may be implicated.

Purpose of the Study:

• To investigate abnormalities in vagal cardiopulmonary baroreflex control of renal sympathetic nerve activity in dogs with left ventricular (LV) dysfunction.
• To determine the relationship between these baroreflex abnormalities and the development of neurohumoral excitation.

Main Methods:

• Serial echocardiography, arterial baroreflex sensitivity testing, and neurohumoral profiling in dogs with progressive LV dysfunction induced by rapid ventricular pacing.
• Assessment of renal nerve activity in response to pulmonary capillary wedge pressure changes in anesthetized dogs.

Main Results:

• Cardiopulmonary baroreflex sensitivity was preserved in mild LV dysfunction but significantly blunted in moderate and severe LV dilatation.
• Arterial baroreflex sensitivity remained intact throughout all stages of LV dysfunction.
• Plasma levels of norepinephrine, renin activity, and arginine vasopressin were unchanged during the initial stages of pacing.

Conclusions:

• Vagal cardiopulmonary baroreflex control of renal sympathetic nerve activity is impaired early in the development of LV dilatation.
• These baroreflex abnormalities precede neurohumoral activation and arterial baroreflex dysfunction in the progression to heart failure.
• Impaired cardiopulmonary baroreflexes become evident as LV end-diastolic volume begins to increase.