SUMMARY1. 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-' 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 2-7 % 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, anuric 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.
Stimulation of the nucleus accumbens evokes a potent inhibition in neurons of the ventral tegmental area. GABA is likely to act as a transmitter in this descending inhibitory system.
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