Abstract
Inflation of a balloon for 2 h at the superior vena caval-right atrial junction of the rat reduced the salt intake of animals that had been sodium and water depleted by peritoneal dialysis with hyperoncotic colloid. After the balloons were deflated, the experimental group drank more than the control group so that the total sodium intake of the two groups was the same. Thus stimulated increased venous return to the heart attenuates salt appetite. Since this phenomenon might be secondary to a reflex reduction in plasma renin activity, the experiment was repeated using a model of salt appetite in which the renin-angiotensin system is known to be suppressed, namely the deoxycorticosterone acetate-treated rat. Salt intake was again significantly reduced by inflation of the right atrial balloon. It is concluded that pathways exist, independent of the renin-angiotensin system, whereby information obtained from the cardiac volume receptors regarding the state of filling of the vasculature may be used to regulate salt intake.
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