Figure 2

Diagram of the potential relationship between peripheral and central renin-angiotensin systems and ADH secretion. Angiotensin II (ANGII) in the peripheral circulation is accessible to circumventricular organs (CVOs), which lack the blood–brain barrier (BBB). Within CVOs, high levels of ANGII (for example, via the infusion of ANGII) can stimulate the ADH secretion via ANGII receptors in the brain. Most of the blood-borne angiotensin I (ANG I) is converted into ANGII at the lungs by the angiotensin-converting enzyme (ACE) under physiological conditions, although the rate of this conversion process is decreased under pathological conditions. Because the activity of ACE in CVOs is much higher than that in the lungs, the redundant ANG I may be converted to ANGII locally and this converted (and high levels of) ANGII may then stimulate the ADH secretion.