Cardiac sympathetic nerve activity (SNA) is an important short term controller of cardiac function and arterial pressure. Studies also suggest that that long-term increases in cardiac SNA may contribute to hypertension, coronary artery disease and cardiac remodeling in heart failure. However, our understanding of the role of cardiac sympathetic nerves in chronic models of cardiovascular disease has been limited by inadequate experimental approaches. The present study was conducted to develop a surgical method to surgically denervate the sympathetic nerves to the rat heart for long-term cardiovascular studies. We characterized the effect of cardiac sympathetic denervation on basal levels of mean arterial pressure (MAP) and heart rate (HR) and the responses to administration of atenolol, a beta-1 adrenoceptor antagonist. Rats were instrumented with telemetry transmitters for continuous recording of MAP and HR. After a 4 day baseline period, rats were subjected to bilateral stellate ganglionectomy (SGX; N=9) or sham surgery (SHAM; N=8). 7 days following SGX or SHAM surgery, rats were administered atenolol for 5 days followed by a 7 recovery period. Following a transient decrease, SGX had no effect on basal MAP but chronically decreased HR compared to baseline and SHAM rats. 5 days of atenolol treatment decreased MAP similarly in SGX and SHAM rats. Atenolol resulted in a marked bradycardia in SHAM rats, but had neglible effects on HR is SGX rats. Measurement of the content of cardiac catecholamines in all cardiac chambers at the end of the study verified successful sympathetic denervation. This study confirms that bilateral stellate ganglionectomy is useful method to study the contribution of cardiac sympathetic nerves to the regulation of cardiac function. Moreover, these results suggest that cardiac sympathetic nerves are relatively unimportant in maintaining the basal level of MAP or the depressor response to atenolol in conscious unrestrained rats.