Key result
Upstream sympathetic activation induced significant upregulation of neuropeptide Y in the left stellate ganglion and cardiac sympathetic nerves, resulting in cardiac dysfunction like stress cardiomyopathy.
Why the study?
Although stress cardiomyopathy and transient LV apical ballooning are severe, their precise underlying mechanisms remain unclear and appropriate animal models are needed.
Upstream sympathetic activation induces significant upregulation of neuropeptide Y in the left stellate ganglion, which interrupts beta-adrenergic signaling and leads to stress cardiomyopathy-like cardiac dysfunction.
Hypothesis-generating for NPY as a stress cardiomyopathy target; human studies needed before any clinical relevance.
Substantial emotional or physical stress may lead to an imbalance in the brain, resulting in stress cardiomyopathy (SC) and transient left ventricular (LV) apical ballooning. Even though these conditions are severe, their precise underlying mechanisms remain unclear. Appropriate animal models are needed to elucidate the precise mechanisms. In this study, we established a new animal model of epilepsy-induced SC. The SC model showed an increased expression of the acute phase reaction protein, c-Fos, in the paraventricular hypothalamic nucleus (PVN), which is the sympathetic nerve center of the brain. Furthermore, we observed a significant upregulation of neuropeptide Y (NPY) expression in the left stellate ganglion (SG) and cardiac sympathetic nerves. NPY showed neither positive nor negative inotropic and chronotropic effects. On the contrary, NPY could interrupt β-adrenergic signaling in cardiomyocytes when exposure to NPY precedes exposure to noradrenaline. Moreover, its elimination in the left SG via siRNA treatment tended to reduce the incidence of SC. Thus, our results indicated that upstream sympathetic activation induced significant upregulation of NPY in the left SG and cardiac sympathetic nerves, resulting in cardiac dysfunctions like SC.
No takes yet. Share an insight, caveat, or question.
Arai et al. (2022) studied Stress (Takotsubo) cardiomyopathy. Epilepsy-induced stress cardiomyopathy model and NPY siRNA vs. Control animals / Control siRNA was evaluated on Incidence of stress cardiomyopathy and NPY expression. Upstream sympathetic activation induced significant upregulation of neuropeptide Y in the left stellate ganglion and cardiac sympathetic nerves, resulting in cardiac dysfunction like stress cardiomyopathy.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: