TABLE 1.

Neurochemical control of cardiovascular disorders.

Disease model	Species	Pathways	Effects	Therapies	References
AF	Human, Rodent, Canine	β–adrenergic stimulation, derangement of the ET-1/NGF pathway	Cardiac autonomic nervous system imbalance, Adrenergic and cholinergic fibers hyper-sprouting, Atria morphological remodeling	β-blockers, Cardiac vagal limb ablation	Swissa et al. (2005), Tan et al. (2008), Xie et al. (2011), Li et al. (2013), Suita et al. (2015)
MI	Human, Rodent, Canine	β–adrenergic hyperstimulation, sinusoidal pattern in NGF expression, inflammatory activity	Early hyperinnervation followed by NGF depletion and myocardial denervation, trans-differentiation of the autonomic cardiac phenotype	β-blockers, ACE inhibitors, NGF receptor (TrkA) antagonist ligands	Kuruvilla et al. (2004), Zhou et al. (2004), Kimura et al. (2010), Shi and Habecker (2012), Li and Li (2015), Olivas et al. (2016)
HF	Human, Rodent, Canine	NE spillover, β–adrenergic signaling dysregulation	Neurotrophic factors decline, TH synthesis inhibition, disruption of cardiac sympathetic fibers, myocardial denervation	β-blockers, ACE inhibitors, Sartans	D'Elia et al. (2014), Lorentz et al. (2013), Krum et al. (2011a), Fowler (2004)
Aging/AD	Human, Rodent	Cerebral Aβ aggregates and tau neurofibrillary tangles, neuroinflammation, cerebral dysfunction, brain neuro-signaling pathway dysregulation	Calcium handling impairment, cardiac chambers dilation, HF	β-blockers, ACE inhibitors, Sartans	Li et al. (2006b), Gianni et al. (2010), Cermakova et al. (2015), Troncone et al. (2016), Sanna et al. (2019), Tublin et al. (2019)

Abbreviations: AF, Atrial Fibrillation; MI, Myocardial Infarction; HF, Heart Failure; AD, Alzheimer’s disease.