Neurohormonal Mechanisms in Heart Failure Management

Heart failure is characterised by the heart’s inability to maintain adequate circulation, prompting compensatory neurohormonal responses that initially support cardiac output but become maladaptive over time. Central to this process are the renin–angiotensin–aldosterone system and the sympathetic nervous system, which drive vasoconstriction, sodium retention and myocardial remodelling. Chronic activation of these pathways leads to progressive ventricular dysfunction, fibrosis and adverse vascular changes. Endogenous natriuretic peptides counterbalance these effects by promoting diuresis, vasodilation and inhibition of fibrosis, yet their efficacy diminishes as the disease advances. Modern management strategies target these hormonal circuits: angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and mineralocorticoid receptor antagonists disrupt renin–angiotensin–aldosterone signalling, while β-blockers attenuate sympathetic overactivity. More recent approaches combine neprilysin inhibition with angiotensin receptor blockade to enhance natriuretic peptide bioavailability. Adjunctive device therapies and lifestyle measures further modulate neurohormonal tone. Ongoing research seeks to refine patient selection, mitigate side effects and explore novel peptides, receptor modulators and anti-inflammatory agents that can restore hormonal equilibrium and improve long-term outcomes on a global scale.

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Neurohormonal Mechanisms in Heart Failure Management publication trend

The graph below shows the total number of articles in neurohormonal mechanisms in heart failure management across all publications each year (not limited to Nature Index journals).

Technical terms

Neurohormonal activation: The release of hormones and neurotransmitters that regulate vascular tone, sodium balance and cardiac contractility in response to reduced perfusion.

Renin–angiotensin–aldosterone system (RAAS): A hormonal cascade that increases blood pressure and volume through angiotensin II-mediated vasoconstriction and aldosterone-driven sodium retention.

Sympathetic nervous system (SNS): The branch of the autonomic nervous system that releases noradrenaline to raise heart rate, contractility and peripheral resistance.

Natriuretic peptides: Cardiac-derived hormones, including atrial and B-type peptides, that promote vasodilation, natriuresis and inhibit fibrosis to counteract volume overload.

β-adrenergic receptors: Cell-surface proteins in the heart and vasculature responsive to sympathetic catecholamines, mediating increased contractility and heart rate.

References

1. Endothelial, Vascular and Sympathetic Alterations as Therapeutic Targets in Chronic Heart Failure. Biomedicines (2023).
2. Emerging Role of Natriuretic Peptides in Diabetes Care: A Brief Review of Pertinent Recent Literature. Diagnostics (2024).
3. A Systematic Review Concerning the Relation between the Sympathetic Nervous System and Heart Failure with Preserved Left Ventricular Ejection Fraction. PLOS ONE (2015).
4. The Sympathetic Nervous System in Hypertensive Heart Failure with Preserved LVEF. Journal of Clinical Medicine (2023).
5. A comprehensive review of heart failure: Unraveling the etiology, decoding pathophysiological mechanisms, navigating diagnostic modalities, exploring pharmacological interventions, advocating lifestyle modifications, and charting the horizon of emerging therapies in the complex landscape of chronic cardiac dysfunction. Medicine (2024).