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2000). These findings suggest that the neurohumoral and pressor responses to changes in cerebrospinal fluid [Na+] are mediated by Na+ sensors located in the lamina terminalis, and that the pathway includes an AT1 receptor. Since angiotensin has an excitatory action on the lamina terminalis (McKinley et al. 1995) and both hypertonic saline and Ang II inhibited RSNA, there must be a later inhibitory synapse in the pathway to the renal nerves, although not in that to the cardiac sympathetic nerves (Fig. 2). The neural pathways have not been fully established, but transneural tracing studies with a neurotrophic virus in rats demonstrate the existence of polysynaptic neural links to the kidney from the rostral ventrolateral medulla, paraventricular nucleus of the hypothalamus (PVN) Cobimetinib molecular weight and lamina terminalis (Sly et al. 1999), and it has been shown that these neurons can be influenced by hypertonic saline and Ang II (Sly et al. 2001). Numerous studies indicate that the PVN plays an important role in cardiovascular and fluid homeostasis, and has anatomical and functional links to the lamina terminalis. Importantly, it was demonstrated recently that the increase in mean arterial pressure and decrease in RSNA in response to i.c.v. hypertonic saline were inhibited by microinjection of the inhibitory amino ALG1 acid, glycine, bilaterally into the PVN in conscious sheep (Fig. 3; Frithiof et al. 2009). This finding indicates that the PVN plays a critical role in cerebrally induced homeostatic responses to elevated [Na+]. These studies indicate that an increase in brain [Na+] leads to a centrally mediated patterned neurohumoral selleck compound response to restore fluid and electrolyte balance. There is evidence that the increased arterial pressure is mediated by the sympathetic nervous system, not arginine vasopressin (Shi et al. 2007), suggesting that SNA is increased to other organs in addition to the heart. The renal sympathoinhibition that we observed would appear to be the logical homeostatic response to a sodium load, since it will promote reduced renin secretion, renal vasodilatation and renal sodium excretion. As well as acting in an organ-specific manner to maintain normal function, the sympathetic nervous system is activated in a differential manner in pathological situations, including heart failure (HF), myocardial infarction, renal failure, hypertension and obesity (Hasking et al. 1986; Grassi et al. 1998; Rumantir et al. 1999; Park et al. 2008). These findings have led to a growing appreciation of the important role of the sympathetic nervous system in a variety of disease states. In HF, cardiac noradrenaline spillover is elevated more than that from kidneys, lungs, gut or liver (Hasking et al. 1986), and the elevation in cardiac noradrenaline spillover occurs earlier in the development of HF than that from other organs (Rundqvist et al. 1997).