Regional changes in rat brain angiotensinogen following bilateral nephrectomy.

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Abstract
One approach to establish the existence and functionality of a brain angiotensin system is to demonstrate selective alterations in that system following perturbation of peripheral cardiovascular functions. The present study utilized this approach to quantify regional angiotensinogen levels in the rat brain following bilateral nephrectomy, a perturbation that severely disrupts salt and water homeostasis. Angiotensinogen, the precursor of any centrally-derived angiotensin, was analyzed since it should provide a marker for a putative angiotensin peptidergic system. Net brain angiotensinogen was determined by correcting total tissue concentrations of angiotensinogen with accurate values of contaminating plasma angiotensinogen. The latter was determined by quantifying regional plasma space utilizing tritiated inulin as a marker of cerebral vascular space. It was found that there were no detectable alterations in regional net brain angiotensinogen in the first 24 hours following nephrectomy despite over a twofold increase in plasma angiotensinogen and the absence of significant plasma renin. By 32 hours postnephrectomy, certain areas of the rat hypothalamus and midbrain exhibited significant elevations in net angiotensinogen content. These areas coincided with regions traversed by neural pathways shown to mediate angiotensin-induced drinking or blood pressure elevations. The results lend further support to the concept of an independent brain angiotensin system.