Abstract 421: The Subfornical Organ (SFO) Mediates CSF Na+ -induced Pressor Response via Activation of AT1 Receptors
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 AT1 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 AT1 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 AT1 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.
- © 2012 by American Heart Association, Inc.