Role of angiotensin II type 1 receptors in the subfornical organ in the pressor responses to central sodium in rats

• Intra-SFO infusion of Na+-rich aCSF causes [Na+]-related increases of BP.
• Intra-SFO infusion of mannitol with the same osmolarity has no effects.
• Intra-SFO infusion of candesartan abolishes pressor response by intra-SFO Na+.
• Intra-SFO candesartan attenuates pressor response to icv infusion of Na+.
• Electrolytic lesion of the SFO similarly attenuates responses to icv Na+.

Central infusion of Na+-rich artificial cerebro-spinal fluid (aCSF) activates the brain renin–angiotensin system and causes sympatho-excitatory and pressor responses. We evaluated the role of the subfornical organ (SFO) and angiotensin II type 1 (AT1) receptors in the SFO in mediating the central Na+-induced pressor response. In conscious Wistar rats, intra SFO infusions of Na+-rich aCSF containing 0.45 and 0.6 M Na+ at 10 nl/min or injection of angiotensin II (Ang II) at 80 ng increased blood pressure (BP) by 15–22 mmHg, whereas mannitol with the same osmolarity as the Na+-rich aCSF had no effects. Intra SFO infusion of the AT1 receptor blocker candesartan abolished the pressor response induced by intra SFO administration of Na+-rich aCSF or Ang II. Intra cerebro-ventricular (icv) infusion of Na+-rich aCSF (0.3 M Na+) at 3.8 μl/min for 10 min increased BP by 15–20 mmHg. Electrolytic lesion of the SFO attenuated these BP increases by 50–70%. Intra SFO infusion of candesartan also prevented 50% of these pressor responses. These data suggest that SFO neurons are indeed sensitive to Na+, the SFO is a major – but not only – site in the brain to sense an increase in CSF [Na+], and activation of AT1 receptors in the SFO mediates the SFO component of the Na+-induced pressor response.