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

Abstract

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. Long-term (7 day) infusions of angiotensin II into the 3rd 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. Intracranial injection or infusion of carbachol caused a transient increase in water intake but had no effect on the intake of 2.7% NaCl. 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. Increased Na appetite was not secondary to increased water intake since it occurred when only 2.7% NaCl was available to drink. Increased Na appetite was not secondary to natriuresis since the angiotensin-stimulated rats went into positive Na balance and, intracranial renin did not cause increased Na excretion in Na-loaded rats and anuric rats showed a significant Na appetite in response to renin. Angiotensin in the brain may play a role in the development of Na appetite.