Opioidergic manipulations affect intake of 3% NaCl in sodium-deficient rats.

On six weekly occasions, a 3% NaCl solution was presented along with water to rats for 2 h 1 day after being treated with furosemide, a diuretic/natriuretic drug that causes a strong hunger for 3% NaCl. On some of the days, the sodium-hungry rats were injected with morphine in doses ranging from 0.3 to 10.0 mg/kg. Morphine produced biphasic effects on intake of 3% NaCl, with doses of 0.3-3.0 mg/kg increasing intakes dose dependently and 10.0 mg/kg decreasing intakes. The 3.0-mg/kg dose nearly doubled rats' mean intake of 3% NaCl. In contrast, naltrexone, an opioid receptor antagonist, reduced intake of 3% NaCl about 25-40% across doses ranging from 0.1 to 10.0 mg/kg. At some doses of morphine and naltrexone, NaCl ingestion was affected without significant influence of water intake. Therefore, it can be inferred that endogenous opioidergic systems participate in the control of NaCl drinking by sodium-deficient rats. The range of demonstrations of opioid involvement in the control of ingestion can now be extended to the hunger for hypertonic NaCl induced by sodium depletion.