Opioid mechanisms are involved in the control of water and NaCl intake and opioid receptors (ORs) are present in the central nucleus of the amygdala (CeA), a site of important facilitatory mechanisms related to the control of sodium appetite. Therefore, in the present study we investigated the effects of the activation of μ-ORs in the CeA on 0.3 M NaCl and water intake in rats. Male Sprague-Dawley rats with stainless steel cannulas implanted bilaterally in the CeA were used. In rats submitted to water deprivation-partial rehydration, bilateral injections of the selective μ-OR agonist [D-Ala², N-Me-Phe⁴, Gly⁵-ol]-enkephalin (DAMGO) in the doses of 1, 2, and 4 nmol into the CeA induced a dose-related increase of 0.3M NaCl intake and water intake, and bilateral injections of the selective μ-OR antagonist D-Phe-Cys-Trp-Arg-Thr-Pen-Thr-NH₂ (CTAP) in the doses of 0.5, 1, and 2 nmol into the CeA produced a dose-related decrease of 0.3 M NaCl and water intake induced by DAMGO 2 nmol into the same site. In rats treated with the diuretic furosemide (10 mg/kg b.w.) combined with the angiotensin-converting enzyme inhibitor captopril (5 mg/kg b.w.) injected subcutaneously, bilateral injections of DAMGO 2 nmol into the CeA increased 0.3 M NaCl intake and water intake and the blockade of μ-ORs with CTAP 1 nmol injected into the CeA reduced the increase in 0.3 M NaCl intake and water intake induced by DAMGO 2 nmol into the same site. Bilateral injections of DAMGO into the CeA did not change urinary volume, sodium urinary excretion and mean arterial pressure, but increased activity. Thus stimulating μ-ORs in the CeA increases hypertonic sodium intake, whereas antagonizing these sites inhibits hypertonic sodium intake. Together, our results implicate μ-ORs in the CeA in a positive regulation of sodium intake.