Figure 8.

Mechanisms involved in the pressor response induced by Ang II and CP55940. Ang II, via AT₁ receptors, leads to endocannabinoid formation in the paraventricular nucleus of hypothalamus (PVN). Endocannabinoids in turn inhibit GABA release by activation of CB₁ receptors. Since little GABA is released, much glutamate (Glu) can be released, also since facilitatory AT₁ receptors on the glutamatergic neuron further increase Glu release. The extents of Glu release and of the pressor response are correlated. The pressor response in SHR increased since AT₁ and CB₁ receptor density in their PVN increased. On the other hand, the pressor response induced by Ang II can be attenuated by CB₁ receptor antagonist AM251. In addition, the pressor response induced by the CB₁ receptor agonist CP55940 can be antagonized by AT₁ receptor antagonist losartan.