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The **cardiac autonomic nerves** are not a single molecular target but rather groups of nerve fibers that make up the cardiac autonomic nervous system (cANS), responsible for regulating the heart’s rate, rhythm, and contractility via sympathetic and parasympathetic divisions[1][3][4][5]. Sympathetic cardiac nerves increase heart rate and contraction force, while parasympathetic (mainly vagal) nerves slow the heart rate and reduce contraction force[3][5]. The autonomic regulation is mediated by neurotransmitters (e.g., norepinephrine, acetylcholine) acting on cardiac adrenoceptors (beta-adrenoceptors) and muscarinic receptors, but the nerves themselves are not receptors, channels, or enzymes—they are anatomical and functional pathways composed of multiple cell types and molecular targets[1][3][5][6]. Disruption of cardiac autonomic activity or structure is implicated in various cardiovascular diseases, especially arrhythmias and sudden cardiac death[1][4]. Key context and limitations: “Cardiac autonomic nerves” is anatomically descriptive and not a single molecular entity, receptor, or canonical target typically recognized in drug discovery. The "target" comprises bundles of sympathetic and parasympathetic nerve fibers containing many molecular targets (e.g., beta-adrenergic receptors, muscarinic receptors) but is not itself a therapeutic target molecule[1][4][5]. If a molecular target is required (e.g., for drug binding), specify the neurotransmitter receptor (such as “Beta-1 adrenergic receptor”) rather than the nerve bundles[3][5][6]. Summary of why "is_incorrect: true": “Cardiac autonomic nerves” is a structural/functional anatomical terminology, not a single molecular or protein target; thus, it does not fit the criteria for a canonical drug target (i.e., receptor, ion channel, enzyme, etc.), even though drugs modulate their function by acting on the receptors and molecules expressed by or within these nerves[1][3][5].
Modulation of sympathetic or parasympathetic tone (e.g., beta-adrenoceptor blockade, muscarinic receptor antagonism, nerve ablation)
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