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1.  Chronic Electrical Stimulation of the Carotid Sinus Baroreflex Improves LV Function and Promotes Reversal of Ventricular Remodeling in Dogs with Advanced Heart Failure 
Circulation. Heart failure  2010;4(1):65-70.
Background
Autonomic abnormalities exist in heart failure (HF) and contribute to disease progression. Activation of the Carotid sinus baroreflex (CSB) has been shown to reduce sympathetic outflow and augment parasympathetic vagal tone. This study tested the hypothesis that long-term electrical activation of carotid sinus baroreflex improves left ventricular (LV) function and attenuates progressive LV remodeling in dogs with advanced chronic HF.
Methods and Results
Studies were performed in 14 dogs with coronary microembolization-induced HF (LV ejection fraction, EF ~25%). Eight dogs were chronically instrumented for bilateral CSB activation using the Rheos® System (CVRx® Inc., Minneapolis, MN) and 6 were not and served as controls. All dogs were followed for 3 months and none received other background therapy. During follow-up, treatment with CSB increased LV EF 4.0 ± 2.4 % compared to a reduction in control dogs of −2.8 ± 1.0% (p<0.05). Similarly, treatment with CSB decreased LV end-systolic volume −2.5 ± 2.7 ml compared to an increase in control dogs of 6.7 ± 2.9 ml (p<0.05). Compared to control, CSB activation significantly decreased LV end-diastolic pressure and circulating plasma norepinephrine, normalized expression of cardiac β1-adrenergic receptors, β-adrenergic receptor kinase and nitric oxide synthase and reduced interstitial fibrosis and cardiomyocyte hypertrophy.
Conclusions
In dogs with advanced HF, CSB activation improves global LV function and partially reverses LV remodeling both globally and at cellular and molecular levels.
doi:10.1161/CIRCHEARTFAILURE.110.955013
PMCID: PMC3048958  PMID: 21097604
heart failure; ventricular remodeling; gene expression; baroreflex function
2.  PROLONGED ACTIVATION OF THE BAROREFLEX DECREASES ARTERIAL PRESSURE EVEN DURING CHRONIC ADRENERGIC BLOCKADE 
Hypertension  2009;53(5):833-838.
Previous studies suggest that prolonged electrical activation of the baroreflex may reduce arterial pressure more than chronic blockade of α1-and β1,2-adrenergic receptors. To determine whether central inhibition of sympathetic outflow has appreciable effects to chronically reduce arterial pressure by actions distinct from well established mechanisms, we hypothesized that chronic baroreflex activation would lower arterial pressure substantially even during complete α1-and β1,2-adrenergic receptor blockade. This hypothesis was tested in 6 dogs during adrenergic blockade (18 days) with and without electrical activation of the carotid baroreflex (7 days). During chronic adrenergic blockade alone, there was a sustained decrease in mean arterial pressure of 21±2 mm Hg (control = 95±4 mm Hg) and nearly a 3-fold increase in plasma norepinephrine concentration (control = 138±6pg/mL), likely due to baroreceptor unloading. In comparison, during adrenergic blockade + prolonged baroreflex activation, plasma norepinephrine concentration decreased to control levels and mean arterial pressure fell an additional 10±1 mm Hg. Because of differences in plasma norepinephrine concentration, we also tested the acute blood pressure lowering effects of MK-467, a peripherally acting α2-antagonist. After administration of MK-467, there was a significantly greater fall in arterial pressure during adrenergic blockade (15±3 mm Hg) than during adrenergic blockade + prolonged baroreflex activation (7±3 mm Hg). These findings suggest that reflex-induced increases in sympathetic activity attenuate reductions in arterial pressure during chronic adrenergic blockade and that inhibition of central sympathetic outflow by prolonged baroreflex activation lowers arterial pressure further by previously undefined mechanisms, possibly by diminishing attendant activation of postjunctional α2-adrenergic receptors.
doi:10.1161/HYPERTENSIONAHA.109.128884
PMCID: PMC2698596  PMID: 19273736
baroreflex; arterial pressure; sympathetic nervous system; α-and β-adrenergic receptors; norepinephrine; renin-angiotensin system

Results 1-2 (2)