Increased sodium appetite in the rat induced by intracranial administration of components of the renin‐angiotensin system.

Intracranial injections of components of the renin-angiotensin system in rats in normal water and Na balance caused an immediate thirst followed by a progressive increase in Na appetite during a test session which lasted 18 h. The effect on water and Na intake was dose-dependent. 2. Long-term (7 day) infusions of angiotensin II into the third cerebral ventricle at rates of 1 or 10 pmol h-1 produced large and sustained increases in intake of water and 2 . 7% NaCl. Intakes sometimes exceeded 100 ml 2 . 7% NaCl per day but quickly fell to normal when the infusion was stopped. 3. Intracranial injection or infusion of carbachol caused a transient increase in water intake but had no effect on the intake of NaCl. 4. The Na appetite induced by intracranial injection of angiotensin was specific for Na since rats offered a choice of water and equimolar concentrations of NaCl and KCl took only water and NaCl. This resembles the pattern seen in Na-depleted rats. 5. Increased Na appetite was not secondary to increased water intake since it occurred when only 2 . 7% NaCl was available to drink. 6. Increased Na appetite was not secondary to natriuresis since, first, the angiotensin-stimulated rats went into positive Na balance, secondly, intracranial renin did not cause increased Na excretion in Na-loaded rats and thirdly, anureic rats showed a significant Na appetite in response to renin. 7. These results suggest that angiotensin in the brain may play a role in the development of Na appetite.