Objective      To determine the alteration of cardiac sympathetic norepinephrine transporter (NET)

nerve growth factor (NGF) and neurotrophin receptor TrkA in cardiac sympathetic nerve of rats under long-term pressure overload (POL) induced by suprarenal abdominal aortic constriction (AC) in order to elucidate the mechanisms of cardiac sympathetic nerve remodeling.       Methods      Forty adult Wistar rats weighing 156±10 g were divided into sham-operation (n=10) and POL groups (n=30) randomly. In 8 weeks after AC

the model establishment was identified

transthoracic echocardiography and heart weighting were performed

myocardial NGF protein were determined by immunofluorescence staining

and mRNA levels of NET in cardiac sympathetic ganglia

and TrkA and growth associated protein 43 (GAP-43) in myocardial tissues were determined by real-time PCR.       Results      POL induced obvious cardiac hypertrophy

with increased interventricularseptal thickness during systole (IVSs)

diastolic LV posterior wall thickness (LVPWd)

and interventricularseptal thickness during diastole (IVISd). The left ventricular mass index (LVMI) was elevated by 33.23%

and heart function was enhanced also by increased ejection fraction (EF) and LV endocardial fractional shortening (FS%) compared with sham-operation rats (P0.05). All these indicated that POL resulted in cardiac functional compensation in rats. POL also induced significantly increase of myocardial NGF protein expression (P0.05)

but no difference in the sympathetic NET and myocardial GAP-43 mRNA levels (P0.05)

but obviously decreased expression of TrkA mRNA expression (P0.05) compared with sham-operation rats.       Conclusion      Myocardial lower expression of TrkA might restrain cardiac sympathetic nerve sprouting even in high myocardial NGF protein level induced by POL

and abnormality of post-transcription possibly relate to the dysfunction of NET in heart failure.