The role of catecholamines in central antidiuretic and pressor mechanisms

Angiotensin II (AII), when delivered intraventricularly (IVT) produces an increase in blood pressure and release of antidiuretic hormone (ADH). In the experiments reported here we have investigated the role of central catecholamines in these responses. After central 6-hydroxydopamine (6-OHDA) treatment IVT, AII was less effective in producing a blood pressure increase or ADH release. Similar responses to IVT carbachol were also inhibited. Pressor responses to IVT phenylephrine were not significantly changed after 6-OHDA treatment although ADH release was decreased. In further analysis, both a dopamine blocker, haloperidol, and phentolamine, an α-adrenergic blocker inhibited the pressor response but not ADH release to IVT AII. Both effects may be explained by α-adrenergic blockade. Dopamine IVT alone was ineffective in producing either ADH release or a blood pressure increase and phenylephrine in high doses produced both effects. We conclude that noradrenergic mechanisms may be important as a common mediator of central sympathetic outflow. The ADH release produced by AII and carbachol may be by direct action of periventricular receptors which can be damaged non-specifically by 6-OHDA.