Systemic angiotensin II alters intrinsic heart rate through central mechanisms.

Abstract Angiotensin II (ang II)-induced increases in intrinsic heart rate (IHR), and the resulting tachycardia, may contribute to development of renal hypertension. Whether circulating ang II affects the cardiac pacemaker through peripheral mechanisms or through actions in the central nervous system (CNS) has not been directly tested. These studies determined the role of a central site of ang II action, the tissue surrounding the anteroventral third ventricle (AV3V), in increased IHR induced by systemic ang II. Blood pressure and heart rate were measured in male rats with lesions of the AV3V region and in control-operated animals during i.v. infusion (3 h) of ang II, norepinephrine, or vehicle. IHR was evaluated at the end of the infusion period. Systemic ang II increased blood pressure equally in both experimental groups. However, heart rate was reduced only in animals with AV3V lesions. Furthermore, ang II increased IHR only in control-operated rats. Changes in blood pressure, heart rate, and IHR in response to norepinephrine infusion were similar between animals with AV3V lesions and control-operated rats. These data demonstrate that systemic ang II mediates IHR through actions in the CNS, specifically the AV3V region.