Neuroendocrine mechanisms of left ventricular dysfunction stimulated by anger stress in rats with atherosclerosis--a putative role of natriuretic peptide

ABSTRACT

OBJECTIVE@#To investigate the role of natriuretic peptide in the process of left ventricular dysfunction caused by emotional stress.@*METHODS@#Adult male SD rats (n=30) and Wistar rats (n=60) were selected in this study. Atherosclerosis models were induced with high-fat diet and excess VD3 injection (eight consecutive weeks), and anger stress models were prepared by resident-intruder stress experiment (two consecutive weeks). Furthermore, left ventricular functions were examined by high-resolution echocardiograph, after which left ventricular myocardium and coronary arteries were prepared for pathological section and observed with electron microscope. At the same time, the hypothalamus, medulla oblongata and left ventricular myocardium were also prepared for pathological sections to detect the localization and expression of ANP, BNP and NPR-A with immunofluorescence and western blot.@*RESULTS@#We found that left ventricular functions of atherosclerosis or emotional stress modeled rats were both inferior to the healthy ones and superior to the combined (atherosclerosis and emotional stress) modeled ones (P<0.05). We also found that atherosclerosis and emotional stress could both cause morphological changes of left ventricular cells and capillary which contribute to apoptosis and hyperblastosis. Further more, there was NPR-A distributed in hypothalamus, medulla oblongata, as well as left ventricular tissues with the same express trend between groups, with atherosclerosis modeled rats the highest and the healthy rats the lowest.@*CONCLUSIONS@#The results of our study suggest that anger stress could cause an excess consumption of ANP, BNP and NPR-A in nervous and cardiovascular system which inhibit the compensatory self-repair function of atherosclerosis rats, leading to a promotion of fibrosis and lipid peroxidation, offering insight into the neuroendocrine mechanisms of left heart function obstacle.