Stress, endogenous opioids and salt intake

• Published in: Appetite Vol. 5; no. 1; pp. 53 - 60
• Main Authors: Kuta, C.C, Bryant, H.U, Zabik, J.E, Yim, G.K.W
• Format: Journal Article
• Language: English
• Published: England 01.01.1984
• Subjects: Angiotensin II - administration & dosage; Angiotensin II - antagonists & inhibitors; Animals; Captopril - pharmacology; Drinking - drug effects; Endorphins - antagonists & inhibitors; Endorphins - physiology; Food Deprivation - physiology; food intake; Injections, Intraventricular; Male; Mice; Morphine - pharmacology; Naloxone - pharmacology; obesity; opium; psychological stress; Saline Solution, Hypertonic - pharmacology; salt; Sodium Chloride - pharmacology; Stress, Physiological - physiopathology
• ISSN: 0195-6663; 1095-8304
• DOI: 10.1016/S0195-6663(84)80050-1

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.