Arousal of a specific and persistent sodium appetite in the rat with continuous intracerebroventricular infusion of angiotensin II.

Abstract

SUMMARY1. Prolonged exposure of the brain of the normal Na-replete rat to angiotensin II produced a marked and persistent Na appetite. In a first series of experiments, short-term, repeated systemic injections of isoprenaline or renin (both of which raise circulating angiotensin levels), and repeated intracranial injections of angiotensin II evoked increased ingestion of 2-7 % NaCl. In the second series of experiments, continuous infusions of angiotensin II directly into the brain evoked extremely large intakes of 3 % NaCl.2. In addition to large intakes of hypertonic NaCl some rats drank daily volumes of water that exceeded their body weight.3. Not only did the animals drink large volumes of 3 % NaCl during continuous angiotensin II infusion, but after termination of the infusion they continued to ingest NaCl at a rate comparable to that of the adrenalectomized rat. In most of the animals the persistent NaCl intake diminished over several days, but other animals continued to drink NaCl for as long as their intake was measured (up to 7 months).4. The response to continuous infusion of angiotensin II was dose-dependent.Both water and 3 % NaCl intake increased over a dose range of 6 ng h-1 to 6000 ng h-1.The persistence of the sodium appetite was also dose-dependent across the same range of doses. 5. Angiotensin-induced salt appetite is specific for Na. Animals did not drink 0.5 M-NH4CI and only occasionally drank minimal amounts of 0 5 M-KCl during continuous infusion. 6. The large water turnover was not responsible for the Na appetite. Rats given access to 3 % NaCl only during infusion of angiotensin drank copiously. Animals that were not infused but were given saccharine-flavoured water in order to increase their water intakes did not drink 3 % NaCl offered at the same time even though fluid intake was high. Rats that did not receive intracranial infusions but were infused intragastrically with volumes of water equal to or exceeding the amounts that were drunk during angiotensin infusion did not drink the 3 % NaCl but did drink some water.

Centrally infused atrial natriuretic polypeptide attenuates exaggerated salt appetite in spontaneously hypertensive rats.

“…Preference for salt in rats was reported to be elicited by a variety of experimental interventions; adrenectomy, salivarectomy, ICV administration of angiotensin II, treatments with angiotensin-converting enzyme inhibitors, relatively high doses of deoxycorticosterone acetate, diuretics, and so forth. 2 In the enhancement of salt preference, peripherally, the salivary sodium concentration, which modulates the gustatory input to the central nervous system, and plasma aldosterone level, and centrally, the brain renin-angiotensin system (RAS) 27 may be involved.…”

Increased sodium appetite and polydipsia induced by partial aortic occlusion in the rat.

“…The possible role of angiotensin in sodium appetite is less clear. There is good evidence that angiotensin infused directly into the brain stimulates sodium appetite (Avrith & Fitzsimons, 1980;Bryant, Epstein, Fitzsimons & Fluharty, 1980). However, unless there is a coexisting hypovolaemia, presumably providing a neural signal to sodium appetite, circulating angiotensin seems rather ineffective at stimulating increased intake of NaCl.…”

Richter and sodium appetite: From adrenalectomy to molecular biology

“…Previous studies had shown that central administration of angiotensin II elicited a robust water intake that was followed by a modest salt appetite (Bryant et al, 1980;Buggy & Fisher 1974). Central administration of angiotensin II had also been shown to cause activation of oxytocinergic neurons in the hypothalamus (Ferguson & Kastings, 1988).…”