This review provides a synopsis of the physiologic role of central angiotensin III (AIII), the biologically active degradative product of angiotensin II, in dipsogenesis. The integrity of the central noradrenergic system is essential to the elicitation of polydipsia by AIII. It is conceivable that synaptically released norepinephrine may act on the α1-adrenoceptors to potentiate the drinking response to the heptapeptide. This release, however, may be subjected to a tonic inhibition by the α2-adrenoceptors. Chronic intracerebroventricular administration of AIII fails to produce sustained drinking behavior in spontaneously hypertensive rats. Behavioral and electrophysiologic observations suggest that this is because ofthe development of early desensitization of at least the angiotensin receptors at the subfomical organ, a major target site for AIII-induced dipsogenesis. This process is exacerbated by a suggested dysfunction of the central degradative enzyme for AIII in this strain of rat. Recent results suggest that it is likely that neurons in the caudal hypoglossal nucleus may serve as the final common pathway for AIII-induced drinking response. Furthermore, an excitatory Iink between the nucleus reticularis gigantocellularis in the medulla oblongata and caudal hypoglossal nucleus may form part of the descending neural pathways that mediate the dipsogenesis elicited by AIII. It is evident that AIII in the brain participates actively in at least the initiation and consummatory phases of water homeostasis. Thus, apart from directly acting on the central machinery for circulatory control, AIII may also influence cardiovascular functions by affecting cardiac output via regulation of fluid volume.
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