AVP and hypertensive disorder: As such, the access of blood-borne AII and AVP to nodose ganglion cells in 2K-1C animals would have the capacity to modulate vagal afferent activity and therefore the expression of hypertension and disturbances in baroreceptor reflex function in these animals (see [1, 2, 21, 22]) and perhaps affect the ability of nodose ganglion cells to synthesize AII and AVP receptors designated for deposition onto the cell membranes of the afferent cell bodies and for axonal transport to central and/or peripheral terminals (see [7, 8, 59]).