Abstract
Background: Abrupt conditional changes can interfere with the harmony between the brain and the heart, thereby following impaired cardiovascular function. Stress cardiomyopathy (SC) is a typical sample. SC is a disorder associated with transient left ventricular apical ballooning that is induced by stress. The precise molecular mechanisms of SC remain unclear. Methods and results: (1) By analyzing a new animal model of SC in rodents inducing by epilepsy, we demonstrated hypothalamic activation due to Ccl2 causes LV dysfunction like SC. (2) Upstream sympathetic activation induces strong upregulation of neuropeptide Y (NPY) expression in the left stellate ganglion (LSG) and LV sympathetic nerves. (3) NPY reduced the frequency of Ca2+ sparks when co-injected with noradrenaline in the ventricular myocytes of adult rat. (4) We demonstreted that NPY reduced the contraction of ventricular myocytes of neonatal rat when co-incuvated with noradrenaline by using phase-contrast microscopy. (5) NPY injection into the LSG induces SC-like LV wall motion. (6) The incidence of SC was less frequent in NPY-/- mice than in NPY+/+ mice. Conclusions: Our results demonstrate how brain activation translates into molecular signals in the cardiac nervous system and leads to LV apical ballooning.
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