Stress, endogenous opioids and salt intake.

The effect of stress on NaCl intake was examined in mice given a choice of water and 1.5% NaCl to drink. Immobilization of mice for 15-min and 24-h food deprivation resulted in a 2.5- and 5-fold increases in NaCl intake, respectively, without affecting water intake. Naloxone treatment (0.01, 0.1 and 1.0 mg/kg) produced a dose-dependent decrease in the stress-induced NaCl intake, as did captopril treatment (5, 10 and 50 mg/kg). Intraventricular injection of angiotensin II in mice resulted in an increase in 1.5% NaCl intake, which was blocked by naloxone. Morphine (10 mg/kg) increased the preference of mice for a normally aversive 3.0% NaCl solution, but not for preferred, less concentrated, solutions of NaCl. The results suggest that both endogenous opioids and angiotensin II contribute to stress-induced NaCl intake, and that endogenous opioids may also mediate the increase in NaCl intake, observed with angiotensin II.