Neuropeptide Y modulation of sympathetic activity in myocardial infarction

Objectives. We examined the possible effect of neuropeptide Y in modulating central sympathetic activity after myocardial infarction in rats. Background. Previous studies have shown the coexistence of neuropeptide Y and norepinephrine in the brain and possible functional interaction between the two. Neuropeptide Y inhibits the release of norepinephrine at the presynaptic level and can be considered to act as neuromodulator. Methods. Two groups of rats were examined in this study—an experimental group, defined as those rats undergoing left coronary artery ligation, and sham group without coronary artery ligation, serving as the control group. The animals in both groups underwent microdialysis in the paraventricular nucleus at 2, 4 and 8 weeks after operation. Microdialysis samples were collected with and without injecting neuropeptide Y in the paraventricular nucleus. The concentration of norepinephrine was determined by injecting purified microdialysate samples during high performance liquid chromatography. To explore the receptorʹs possible role, autoradiographic localization of neuropeptide Y receptors in the paraventricular nucleus was also carried out in the experimental and sham groups. Results. The concentration of norepinephrine measured in the samples was decreased by 50% with neuropeptide Y in 2− and 4-week old rats after infarction. but by only 20% (p < 0.05) in 8-week old rats after infarction. The diminished inhibitory effects of neuropetide Y on norepinephrine release was associated with increased sympathetic activity, as reflected by plasm norepinephrine; 8-week old rats after infarction had almost 100% (p < 0.05) increase in their plasm norepinephrine level compared with the sham group. Autoradiography revealed significant decrease in density of neuropeptide Y receptors in the paraventricular nucleus in 8-week old rats after infarction (p < 0.05). Conclusions. The dat presented in this report suggest that the reduction of the inhibitory activation of neuropeptide Y on sympathetic release may contribute to elevated norepinephrine levels after myocardial infarction.