The haemodynamic burden to the cardiac tissue may lead to activation of neurohormones which will increase muscle mass and shift contractility to the right along the Frank-Starling curve. Pressure over load to heart can be induced experimentally by aortic stenosis. This study aimed to examine the interaction between the sympathetic nervous system and renin angiotensin system in the development and progression of cardiac hypertrophy as a result of aortic banding. 36 male SD rats were recruited and randomized into six sub-groups viz, Normal, Sham-operated, Aortic Banded (AB), Aortic Banded treated with Losartan (ABLOS), Aortic Banded treated with 6OHDA (ABSYMP) and Aortic banded treated with both Losartan and 6OHDA(ABSYMPLOS). Losartan was given per oral at a dose of 10mg/kg while 6OHDA was administered intra peritoneal on day 0 (50mg/kg), day 1 (100mg/kg), day 4 (50mg/kg) and day 7 (50mg/kg) and animals were studied in acute experiment on day 8. Pressure over load was produced by placing a constricting band around the supra renal aorta accessed via a flank incision, under Ketamine + Xylazine (10mg/kg+6mg/Kg i/p). Animals were housed individually for 45 days and fed with commercial rat chow and water ad libitum. On the day of experiment, the rats were anaesthetized using Pentobarbitone Sodium at a dose of 60mg/kg i/p and the right carotid artery and left jugular vein were cannulated using a PP50 cannula. Intravenous administration of vasopressor agents noradrenaline, phenylephrine, methoxamine and angiotensin II produced increases in mean arterial pressure (MAP) which were recorded using PowerLab® data acquisition system. Data were expressed as mean ± s.e.m and statistical analysis was done by two way analysis of variance followed by Bonnferonni Dunn All Means post hoc test at a confidence level of 95%. For all vasoactive agents Normal and Sham operated groups showed no difference in the magnitude of the MAP responses expressed as percentage change (%age). A lower magnitude of increase in mean percentage MAP, in response to all vasoactive agents, was observed in AB group in comparison to the ABSYMP group, AB: 23±1.5, 28±1.8, 7±0.6, 221±1.6 and ABSYMP: 50±2.5, 461±2.6, 11±0.8, 42±3.04. Higher responses were observed in the ABLOS group as compared to AB group upon administration of all adrenergic agonists but not to ANGII. ABLOS: 36±1.1, 35±2.4, 10±0.8, 15±1.05 and AB: 23±1.5, 28±1.8, 7±0.6, 23.±1.6 respectively. In ABLOS group whereby the RAS has been compromised, responses to adrenergic agonists decreased significantly (P<0.05) in comparison to the ABSYMP group showing an increase in the sympathetic tone to normalize the homeostasis, ABLOS: 36±1.1, 35±2.4, 10±0.9, 15±1.05 and ABSYMP: 50±2.5, 47±2.6, 11±0.8, 43±3.04 respectively. In conclusion, the findings were consistent with increased activity of both SNS and RAS in a pressure overload rodent model. In the absence of overactive SNS, activity of RAS was also reduced to a normal level in AB rats, suggesting a positive interaction between the two systems.