Abstract
The β-adrenergic agonist, isoproterenol, is well known to increase water intake within 1 hr of its administration to rats (1,2), One of the major contributory mechanisms to this drink is via isoproterenol-induced release of renin from the kidneys (3,4) and the subsequent elevation of circulating angiotensin II (AII) levels. (See also references 5–7 for other mechanisms). AII, administered either peripherally or into circumventricular brain regions such as subfornical organ or anteroventral third ventricle, is itself a potent dipsogen (8–11). However, the evidence that normal levels of AII in blood gain access to these regions of the brain is not compelling, and the inference that peripheral AII exerts its dipsogenic action by a direct effect on the brain is thus based on indirect evidence. For example, peripheral administration of the competitive AII inhibitor, saralasin (sar1, ala8-AII) inhibits the drinking response to centrally-administered AII (12), and lesions of the circumventricular organs inhibit the drink to peripherally-administered AII (11). Further, the brain has its own intrinsic renin-angiotensin system (13) including high affinity receptors for AII in the circumventricular organs (14), yet the ways, if any, in which the central and peripheral renin-angiotensin systems interact have not yet been elucidated.
Supported by contract NCA2-OR204-101 from NASA, Moffett Field, CA.
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Fregly, M.J., Rowland, N.E. (1986). Role for α2-Adrenoceptors in Experimentally-Induced Drinking in Rats. In: de Caro, G., Epstein, A.N., Massi, M. (eds) The Physiology of Thirst and Sodium Appetite. NATO ASI Series, vol 105. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-0366-5_68
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