It is now recognised that all components of the renin-angiotensin system exists within the brain, renin, angiotensinogen and converting enzyme, indicating that it is possible to generate angiotensin locally within particular neural regions (Wright & Harding, 1997). A high density of angiotensin receptors have been found to exist in many areas involved with cardiovascular control, the nucleus tractus solitarius, caudal and rostral venterolateral medulla, paraventricular nucleus and the concept has developed that angiotensin II may play a role as a neuromodulator or neurotransmitter at these sites. What is unclear at present are the factors that may alter the level of activity of brain angiotensin II and the impact this may have on the reflex regulation of sympathetic outflow. One area of focus has been the importance of the level of dietary sodium intake which has a major impact on the renal renin-angiotensin system. It has been demonstrated in acute studies in anaesthetised rats that administration of angiotensin II or drugs blocking its action into the cerebroventricles or directly into more restricted brain areas has a larger impact in adult rats on a low salt diet for two weeks than in rats fed a high salt diet (DiBona, 2003). Interestingly, other reports have demonstrated that exposure of young animals to a high dietary sodium intake through the period of growth and development caused a small rise in basal blood pressure, but the blood pressure elevation caused by a slow low-dose infusion of angiotensin II icv elicited a marked rise in blood pressure and a renal nerve-dependent antinatriuresis (Camara & Osborn, 1998). This suggested that under these particular circumstances that exposure to a life-long high salt diet enhanced the importance of the brain renin-angiotensin system in the regulation of sympathetic activity, at least to the kidney. Our own studies have been aimed to develop these observations further by determining whether this long term exposure to a high salt diet through the period of growth and maturation altered the impact of brain angiotensin II on the baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate (HR). To do this, rats were fed a 3.1% sodium diet from 4 weeks of age for 7 weeks. At this time they were chronically implanted with arterial and venous cannulae, renal nerve recording electrodes and an icv cannula. Following a 3-day recovery from the surgical procedures, baroreflex gain curves were generated for RSNA and HR before and after an icv injection of losartan which was sufficient to block the drinking response to bolus dose of angiotensin II icv. It was apparent that basal blood pressure, RSNA and gain curve parameters for RSNA and HR were very similar in the rats fed on a regular sodium diet and those fed a high salt diet. Following the icv losartan, the baroreflex gain curves for RSNA and HR were unchanged but in the rats fed a high salt diet, the sensitivity of the baroreflex gain curve for RSNA was elevated by over 30%. These data, generated in conscious unstressed rats show that the chronic elevation of dietary sodium intake over the growth and maturation period results in a relatively normal baroreflex control of RSNA. To a degree, this is achieved by a greater role for the brain renin-angiotensin system in that following blockade of angiotensin receptors, the sensitivity of the baroreflex control of RSNA was enhanced. Interestingly, these observations in the conscious unstressed rat provided with lifelong high dietary salt intake seem to be somewhat different from those obtained in adult rats subjected to a relatively short period of high salt intake. This raises the question as to how the prolonged exposure to high salt during a developing phase alters the role of angiotensin within the brain. Exactly at which specific sites this action of the brain renin-angiotensin system is exerted remains to be evaluated.