In salt-sensitive rats on high salt or rats with icv infusion of Na
+
, the increase in CSF [Na
+
] leads to activation of the brain renin-angiotensin-aldosterone system and thereby to sympatho-excitation and hypertension. We tested whether the SFO and AT
1
receptors in the SFO play a crucial role in mediating the Na
+
-induced responses. In conscious Wistar rats, intra-SFO infusion of Na
+
-rich aCSF increased BP in a dose-related manner, whereas mannitol with the same osmolarity had no effects. Intra-SFO infusion of the AT
1
receptor blocker candesartan (cand.,10 μg) abolished pressor responses to intra-SFO infusion of Ang II (80 ng) or Na
+
-rich aCSF (0.45-0.6 M NaCl), and prevented 50% of the BP increase induced by icv infusion of Na
+
-rich aCSF (0.3 M NaCl, 4 μl/min for 6 min). In another set of Wistar rats, electrolytic lesion of the SFO prevented 50-65% of BP increases induced by icv infusion of Na
+
-rich aCSF or Ang II (5 ng/min). These data suggest that the SFO neurons are Na
+
-sensitive and via AT
1
receptors mediate a major part of the pressor response to CSF Na
+
.
Data=means±SE (n=5-7). *p<.05 vs vehicle or sham lesion.
Assessment of serotonergic system in formation of memory and learning
