Periventricular noradrenergic systems are critical for angiotensin-induced drinking and blood pressure responses.

Deficits in experimentally induced drinking and pressor responses after administration of 6-hydroxydopamine (6-OHDA) into the lateral cerebral ventricle (LCV) have been reported. Questions have arisen, however, as to whether these effects are due to non-specific actions of the neurotoxin and, if specific, whether the depletion of dopamine (DA) or of norepinephrine (NE) is the critical factor for producing the impairments. In the present report methods to deplete brain catecholamine (CA) differentially were employed in order to test the hypothesis that central 6-OHDA injections act on brain CA substrates per se to produce behavioral and physiological response deficits to angiotensin II (ANG II) challenges. The findings support the interpretation that forebrain dopamine is essential for the mediation of sensorimotor integration involved in response to acute homeostatic stressors. In addition, the outcome identifies an important role for forebrain noradrenergic systems in the mediation of ANG II-elicited drinking and blood pressure responses.