The brain renin-angiotensin system importantly regulates blood pressure (BP) and its reflex control. We reported recently that intra-cerebroventricular (icv) administration of the angiotensin type 1 (AT1) receptor antagonist, losartan, increased the sensitivity of the high pressure baroreflex control of renal sympathetic nerve activity (RSNA) in conscious rats (1). The aim of the present study was to investigate whether brain AII influenced the reflex renal sympatho-inhibition arising from stimulation of the low pressure cardiopulmonary receptors in conscious hypertensive as well as normotensive rats. This was done by evaluating the changes in RSNA during VE before and after icv administration of the AT1 receptor antagonist, losartan, in conscious Wistar and SHR. Male Wistar and SHR rats, 260-290g, were anaesthetised with pentobarbital sodium (60 mg/kg ip). The right femoral artery and jugular vein were cannulated. The left kidney was exposed and an electrode sealed onto the renal nerve. Rats were placed into a sterotaxic frame and a guide cannula was implanted into the right lateral cerebroventricle. The animal was then allowed to recover from surgery for at least three days. VE, normal saline given iv at the volume equivalent to 15% of estimated plasma volume (60 ml/kgbwt) over 10 min, was performed before and 20min after the AT1 receptor antagonist, losartan, was given icv at 15µg+7.5µg/h. BP, heart rate (HR) and RSNA were measured before, during, 10 min and 20 min after the VE. Means ±SEM were subjected to ANOVA with significance taken at P<0.05. In normal Wistar rats (n=6), basal BP was 105±3 mmHg, HR 413±17 bpm and RSNA 304.1±100.1 µV/s. VE had no effect on BP or HR, but RSNA fell by 27.4% (P<0.05), which returned to the basal levels 10 min after the end of VE. After 20min of losartan icv, VE decreased RSNA by 44.8% (P<0.05), which was greater (P<0.05) than before losartan icv, and was still 14% below the basal volumes (P<0.05) even 20min after the VE. In the SHR (n=8), BP was 153±5 mmHg, HR 390±13 and RSNA 327.4±77.4µV/s. VE reduced RSNA by 17.8% (P<0.05), which was smaller (P<0.05) than that in Wistar rats. After losartan icv, VE decreased RSNA by 24.5%, which was greater than before losartan. RSNA returned to the basal levels 10 min after VE both before and after losartan icv. The data showed that the renal sympatho-inhibition of VE was enhanced by central administration of AT1 receptor antagonist, losartan. These findings indicate that endogenous AII within the brain has a tonic inhibitory action on the cardiopulmonary reflex in both conscious Wistar and SHR.