We recently reported that acute intermittent hypoxia (AIH, 10x45s of 10% O₂, 5 min intervals) produces LTF of splanchnic sympathetic nerve activity (sSNA), independent of respiratory LTF (Xing & Pilowsky, 2010, J Physiol, 588:3075). We hypothesised that sympathetic LTF (sLTF) is the result of intermittent activation of RAS, by renal hypoxia caused by AIH-evoked hypotension. We recorded phrenic nerve activity (PNA) and sSNA, in anesthetised (pentobarbitone, 60mg/kg, ip), vagotomised, and ventilated Sprague-Dawley rats. Intermittent bolus injections of angiotensin II (Ang, 10x35pmol in 0.1ml, iv), at the same 5 min intervals as AIH, elicited sLTF (+42.4 ±11.5%, n=5). Intermittent phenylephrine (PE, 10x 25μg in 0.1mL, iv) also produced sLTF (+72.4±21.6%, n=5), possibly via renal vasoconstriction induced renin release. Intermittent sodium nitroprusside induced hypotension (10x50μg in 0.1mL, iv) did not elicit sLTF (+2.4±5.6%, n=5). Infusion of Ang (350pmol in 1mL) or PE (250μg in 1mL) over 10 mins, also did not cause sLTF, indicating that intermittent stimulation of RAS is essential for sLTF to develop. PNA was unchanged in all groups. This data supports the idea that sLTF and respiratory LTF are mediated by separate mechanisms and that intermittent stimulation of peripheral RAS may be sufficient to elicit sLTF. This data may be relevant to sympathetic overactivity in sleep apnea patients. Funded by NH&MRC, ARC.