Renin-angiotensin system is believed to have important roles in blood pressure regulation. Baro and chemoreceptor afferents project to the nucleus tractus solitarius (NTS) neurons. The expression of angiotensin II type 1 (AT₁) and 2 (AT₂) receptors in the NTS is confirmed. However the physiological roles of angiotensin II (Ang II) in NTS are not fully understood. We have previously reported that ang II increases the frequency of spontaneous EPSCs (sEPSCs) through the activation of AT₁ receptors and decreases it through AT₂ receptor activation. Contrary, Ang II augmented the amplitude of tractus solitarius evoked EPSCs (eEPSCs) via the activation of AT₂ receptors and decreased it by AT₁ receptor activation. In this report we aimed to reveal the involvement of NO cascade in these effects of Ang II by using a slice patch-clamp technique.
 The prior application of L-NAME inhibited the excitatory effects of Ang II on sEPSCs via AT₁ receptors but not antagonized the inhibitory effects of on sEPSCs via AT₂ receptors. Similarly, prior application of L-NAME antagonized the inhibitory effects of Ang II on eEPSCs via AT₁ receptors but not antagonized the augmenting effects on eEPSCs by AT₂ receptors.
These results suggest that the activation of AT₁ receptors in the NTS induces NO production and produced NO induces facilitation of sEPSCs and inhibition of eEPSCs.