In a preclinical model, Angiotensin II-induced hypertension disrupts cardiac sympathetic innervation, contributing to a heart failure phenotype and increased arrhythmogenesis.
Suggests sympathetic denervation contributes to arrhythmogenesis in hypertensive HF models; leaves open translation to human therapy.
Angiotensin II (ANG II)-induced hypertension leads to a heart failure phenotype and cardiac sympathetic denervation with the endocardial region of the left ventricle being the most affected. Denervation is accompanied by loss of norepinephrine content in the left ventricle and increased premature ventricular contractions (PVCs) after isoproterenol and caffeine injection. ANG II treatment also causes morphological changes in cardiac-projecting left stellate ganglion neurons.
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Scalco et al. (2024) studied this question.
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