FAILURE OF SODIUM LOADING TO INFLUENCE THE CONCENTRATION OF ISO-RENIN IN RAT BRAIN

In addition to its well-known peripheral actions, angiotensin II has been implicated in central nervous mechanisms concerned with the modulation of blood pressure, drinking, the release of antidiuretic hormone (ADH) and the secretion of adrenocorticotrophin(ACTH; see Severs & Daniels-Severs, 1973). The receptors responsible for mediating these central effects are both central and peripheral in relation to the blood\p=n-\brainbarrier. Because angiotensin II does not cross this barrier rapidly (Volicier & Loew, 1971), the physiological significance of the receptive sites for angiotensin II which lie on the central side of the barrier (e.g. in the mid-brain peri-aqueductal grey matter and the supraoptic nucleus of the hypothalamus) is unclear. Recently, an independent iso-renin-angiotensin system has been demonstrated in the central nervous system (for review see Ganten, Hutchinson, Schelling, Ganten & Fisher, 1976) and this discovery, when considered together with the well-known central effects of angiotensin II on hydration, has led to the formulation of attractive hypotheses regarding the participation of the brain iso-renin-angiotensin system in the control of salt and water balance. To study these controversial hypotheses and the relation between the renin systems in the plasma and brain, the effects of drinking sodium chloride solution on the concentra