Water deprivation increases angiotensin-converting enzyme but not AT1 receptor expression in brainstem and paraventricular nucleus of the hypothalamus of the rat

The rostral ventrolateral medulla (RVLM) is critical to the maintenance of blood pressure. It has been proposed that blood-borne Ang II can influence the RVLM via a neural connection between the circumventricular organs and paraventricular nucleus of the hypothalamus (PVH) and that a component of this pathway is angiotensinergic. A period of water deprivation leads to increased ability of angiotensin type 1 (AT1) receptor antagonists to reduce blood pressure when administered into the RVLM and PVH. We studied the differences in AT1 receptor and angiotensin-converting enzyme (ACE) expression in these and other brain regions involved in blood pressure regulation and water intake following dehydration. AT1 receptor and ACE expression in brains of rats deprived of water for 48 h were compared to that of water-replete rats by quantitative receptor autoradiography. AT1 receptor expression was increased in the subfornical organ and periventricular nucleus of the hypothalamus, but not in other brain regions measured. ACE expression was increased in the RVLM, PVH, choroid plexus, median preoptic nucleus, and organosum vasculosum of the lamina terminalis. These findings suggest that increased Ang II production but not increased receptor expression in the PVH and RVLM is the mechanism by which Ang II in the brain helps to sustain systemic blood pressure during periods of water deprivation.