The Parasympathetic Nervous System and Heart Failure: Pathophysiology and Potential Therapeutic Modalities for Heart Failure

Olshansky, Brian; Sullivan, Renee M.; Colucci, Wilson S.; Sabbah, Hani N.

doi:10.1007/978-3-319-15961-4_6

Cited by 80 publications

(121 citation statements)

References 87 publications

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“…Although abundant evidence shows that overactivation of the sympathetic nervous system is associated with a worse outcome in CHF patients (46), involvement of the disordered parasympathetic function in disease progression and prognosis of CHF patients is only beginning to be recognized (44,45).…”

Section: Discussionmentioning

confidence: 99%

Heart failure-induced changes of voltage-gated Ca²⁺ channels and cell excitability in rat cardiac postganglionic neurons

Liu

Zhang

et al. 2014

American Journal of Physiology-Cell Physiology

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Chronic heart failure (CHF) is characterized by decreased cardiac parasympathetic and increased cardiac sympathetic nerve activity. This autonomic imbalance increases the risk of arrhythmias and sudden death in patients with CHF. We hypothesized that the molecular and cellular alterations of cardiac postganglionic parasympathetic (CPP) neurons located in the intracardiac ganglia and sympathetic (CPS) neurons located in the stellate ganglia (SG) possibly link to the cardiac autonomic imbalance in CHF. Rat CHF was induced by left coronary artery ligation. Single-cell real-time PCR and immunofluorescent data showed that L (Ca(v)1.2 and Ca(v)1.3), P/Q (Ca(v)2.1), N (Ca(v)2.2), and R (Ca(v)2.3) types of Ca2+ channels were expressed in CPP and CPS neurons, but CHF decreased the mRNA and protein expression of only the N-type Ca2+ channels in CPP neurons, and it did not affect mRNA and protein expression of all Ca2+ channel subtypes in the CPS neurons. Patch-clamp recording confirmed that CHF reduced N-type Ca2+ currents and cell excitability in the CPP neurons and enhanced N-type Ca2+ currents and cell excitability in the CPS neurons. N-type Ca2+ channel blocker (1 μM ω-conotoxin GVIA) lowered Ca2+ currents and cell excitability in the CPP and CPS neurons from sham-operated and CHF rats. These results suggest that CHF reduces the N-type Ca2+ channel currents and cell excitability in the CPP neurons and enhances the N-type Ca2+ currents and cell excitability in the CPS neurons, which may contribute to the cardiac autonomic imbalance in CHF.

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Section: Discussionmentioning

confidence: 99%

Heart failure-induced changes of voltage-gated Ca²⁺ channels and cell excitability in rat cardiac postganglionic neurons

Liu

Zhang

et al. 2014

American Journal of Physiology-Cell Physiology

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“…2 In the presence of HF, dysregulation of the autonomic nervous system, characterized by increased sympathetic tone and decreased parasympathetic tone, is associated with progressive HF and increased mortality. [3][4][5] An understanding of the pivotal role of the imbalance of the autonomic nervous system in the progression of HF has prompted the development of different nonpharmacologic therapeutic approaches, including vagal stimulation and spinal cord stimulation (SCS), which can modulate cardiac autonomic tone. [6][7][8][9] SCS with an implantable device has been used clinically for more than 30 years to relieve angina symptoms in patients with severe coronary artery disease.…”

Section: Introductionmentioning

confidence: 99%

Thoracic Spinal Cord Stimulation for Heart Failure as a Restorative Treatment (SCS HEART study): First-in-man experience

Tse¹,

Turner²,

Sanders³

et al. 2015

Heart Rhythm

102

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“…The cardiovascular system answers to different stressors through complex dynamic interactions between the sympathetic and parasympathetic components of the nervous system; they modulate heart rate response, cardiac contractility, venous capacitance and tone of resistance vessels [1,2].…”

Section: Introductionmentioning

confidence: 99%

Impact of type of intervention for aortic valve replacement on heart rate variability

Compostella

Russo

Compostella

et al. 2015

International Journal of Cardiology

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The Parasympathetic Nervous System and Heart Failure: Pathophysiology and Potential Therapeutic Modalities for Heart Failure

Cited by 80 publications

References 87 publications

Heart failure-induced changes of voltage-gated Ca²⁺ channels and cell excitability in rat cardiac postganglionic neurons

Heart failure-induced changes of voltage-gated Ca²⁺ channels and cell excitability in rat cardiac postganglionic neurons

Thoracic Spinal Cord Stimulation for Heart Failure as a Restorative Treatment (SCS HEART study): First-in-man experience

Impact of type of intervention for aortic valve replacement on heart rate variability

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The Parasympathetic Nervous System and Heart Failure: Pathophysiology and Potential Therapeutic Modalities for Heart Failure

Cited by 80 publications

References 87 publications

Heart failure-induced changes of voltage-gated Ca2+ channels and cell excitability in rat cardiac postganglionic neurons

Heart failure-induced changes of voltage-gated Ca2+ channels and cell excitability in rat cardiac postganglionic neurons

Thoracic Spinal Cord Stimulation for Heart Failure as a Restorative Treatment (SCS HEART study): First-in-man experience

Impact of type of intervention for aortic valve replacement on heart rate variability

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Product

Resources

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Heart failure-induced changes of voltage-gated Ca²⁺ channels and cell excitability in rat cardiac postganglionic neurons

Heart failure-induced changes of voltage-gated Ca²⁺ channels and cell excitability in rat cardiac postganglionic neurons